The World Health Organisation (WHO), in its quest to find efficacious therapies to treat COVID-19, plans to conduct a multi-arm, multi-country clinical trial. The trials have yet to begin, but ten countries have already signed up. Only one of them, South Africa, is on the African continent.

Of course, the WHO isnt the only organisation trying to find treatments or even a vaccine for COVID-19. The United States National Institutes of Health maintains an online platform that lists all registered, ongoing clinical trials globally. On March 26, a quick search of the platform using the term coronavirus revealed 157 ongoing trials; 87 of these involve either a drug or a vaccine, while the rest are behavioural studies. Only three are registered in Africa all of them in Egypt.

This low representation of African countries in clinical trials is not unusual. Poor visibility of existing sites, limited infrastructure and unpredictable clinical trial regulatory timelines are some of the key issues hindering investments in this area.

Africas virtual absence from the clinical trials map is a big problem. The continent displays an incredible amount of genetic diversity. If this diversity is not well represented in clinical trials, the trial findings cannot be generalised to large populations.

The same goes for the outcomes of the COVID-19 studies. They too may not be relevant for people in African countries unless conducted locally. This is because responses to drugs or vaccines are complicated and can be influenced by, among other things, human genetics: different people will respond differently to different drugs and vaccines.

More countries on the African continent must urgently get involved in clinical trials so that the data collected will accurately represent the continent at a genetic level.

Time is of the essence. The usual approach, of developing site or country specific protocols, wont work. Instead, African governments need to look at ways to harmonise the response towards COVID-19 across the continent. Now, more than ever, African countries need to work together.

Centres of excellence

Africa does have clinical trial infrastructure and capabilities. But the resources remain unevenly distributed. The vast majority are in Egypt and South Africa. Thats because these countries have invested more heavily in research and development than others on the continent.

Traditionally, clinical trials are conducted at centres of excellence, which are sites that have the appropriate infrastructure and human skills necessary to conduct good quality trials. These can be located at a single university or research organisation, or work can be split between a few locations. But setting up these centres requires significant time and financial investment. Most that I am aware of on the continent have developed over the years with heavy support from external partners or sponsors. In many cases, African governments have not been involved in these efforts.

Once such centres are set up, the hard work continues to maintain these centres and to ensure theyre able to attract clinical trial sponsors. They require continuous funding, the establishment of proper institutional governance and the creation of trusted, consistent networks.

Also read: COVID-19: What Are Serological Tests, and How Can They Help India?

Usually African scientists leading clinical trial sites can apply for funding to conduct a trial; if the site is well known the scientists may be approached by a sponsor such as a pharmaceutical company interested in conducting a trial.

Clearly this approach takes time and usually benefits well-known sites or triallists. So what alternatives are available in the face of an epidemic thats moving as fast as COVID-19?

How to change direction

Key stakeholders should work together to expedite the rollout of trials in different countries. This would include inter-country collaborations such as working with different governments and scientists in co-designing trials; and providing harmonised guidelines on patient management, sample collection and tracking and sharing results in real time.

African governments, meanwhile, should provide additional funding to clinical research institutions and clinical trial sites. This would allow the sites to pull resources together and rapidly enrol patients to answer various research questions.

Because of the uneven distribution of skills and resources the continent should also adopt a hub-and-spoke model in its efforts. This would involve countries that dont have much capacity being able to ship samples easily across borders for analysis in a centralised well-equipped laboratory, which then feeds back data to the country of sample origin.

Governments should also form a task force to quickly engage with key pharmaceutical companies with drug candidates for COVID-19. This team should establish the companies appetite for collaborations in conducting relevant trials on the continent.

Through all of this, it is necessary for stakeholders to identify and address key ethical issues that may arise. Ethics should not be compromised by haste.

Beyond COVID-19

Every countrys epidemic preparedness kit should contain funds set aside for clinical trials during epidemics or pandemics.

This would require governments on the continent to evaluate their role and level of investment in the general area of clinical trials. This will augment the quality and quantity of clinical trials in the face of the constant challenge of emerging and re-emerging infectious diseases as well as a steady rise in non-communicable diseases.

On top of this, clinical trial centres, clinical research institutions and clinical triallists on the continent should strive to increase their visibility in the global space. This will make them easy to find in times of crisis, and enhance both south-south and north-south collaborations.

The African Academy of Sciences is currently building an online platform to facilitate this visibility and encourage greater collaboration.

Jenniffer Mabuka-Maroa isProgramme Manager, African Academy of Sciences.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Go here to read the rest:

COVID-19: Few Clinical Trials are Done in Africa. This Needs to Change ASAP. - The Wire

People walk along Harajuku's famous Takeshita Street in Tokyo's Shibuya Ward, on March 28, 2020. (Mainichi/Kimi Takeuchi)

Experts in Japan have been simulating how the spread of the novel coronavirus can be tamped down, but in areas where the national government has declared a state of emergency, people's behavior must be firmly restricted, which is a task that, realistically speaking, is extremely difficult.

Akihiro Sato, a professor of data science at Yokohama City University, analyzed the numbers of 15 prefectures, including the seven where the state of emergency was declared. Based on the number of newly infected people announced by local governments, and the proportion of people who recover after being infected and showing symptoms, Sato calculated the shift in the numbers of people who were infected. Setting behavior before the period in which newly infected people increased by a large margin at 100%, Sato calculated the target percentage at which people must refrain from direct contact with others in the following two weeks for no new infections to be detected in the long term.

The results showed that in the case of Tokyo, every individual would have to cut back on the time spent on public transportation and the people they meet by 98%. For example, if one person rides on trains and buses for a total of seven hours per week, and has direct contact with a total of 100 people through work and leisure activities, that person must cut back their time on public transport to 8.4 minutes and their contact to two people per week to prevent new infections from being detected in the long term.

Fukuoka Prefecture requires the greatest behavioral restrictions, at 99.8%. Professor Sato emphasized, "Similar to evacuating from floods and tsunami, the current infection requires behavior that avoids people."

Meanwhile, Jun Ohashi, an associate professor at the University of Tokyo who specializes in human genetics, took particular note of the behavior of those infected with the new coronavirus who have symptoms and those who do not. Based on global infection data, Ohashi postulated that one person infects, on average, 2.5 people. He then calculated that in a city of 100,000 people, when there is one person who tests positive for the virus, the number of newly infected people in a day will reach 15,700 people at its peak. However, if the person who tests positive for the virus reduces their contact frequency with others by 55% of their usual behavior, newly infected people would drop to 430 people per day.

"Unless everyone, including those who are asymptomatic and those who are not infected, suppress the frequency with which they come into contact with people, the number of people who are infected will continue to rise, possibly causing the collapse of the health care system," Ohashi said. "Until we come up with vaccines and therapeutic medications, a long-term vision is essential, and it is important to change the awareness of each and every individual.

Hiroshi Nishiura, a professor specializing in theoretical epidemiology at Hokkaido University, has also calculated that if person-to-person contact can be reduced by 80%, the number of newly infected people would decline.

(Japanese original by Ryo Watanabe and Ayumu Iwasaki, Science & Medical News Department)

Go here to read the rest:

'Behavioral suppression' needed to decrease coronavirus infections in Japan: experts - The Mainichi

Sam Williams Macaw Recovery Network in Costa Rica rewilds captivity-hatched fledgling scarlet and great green macaws. But introducing young birds into a complex forest world bereft of the cultural education normally provided by parents is slow and risky.

For 30 years or so scientists have referred to the diversity of life on Earth as biological diversity, or just biodiversity. They usually define biodiversity as operating at three levels: the diversity of genes within any particular species; the diversity of species in a given place; and the diversity of habitat types such as forests, coral reefs, and so on. But does that cover it? Not really. A fourth level has been almost entirely overlooked: cultural diversity.

Culture is knowledge and skills that flow socially from individual to individual and generation to generation. Its not in genes. Socially learned skills, traditions and dialects that answer the question of how we live here are crucial to helping many populations survive or recover. Crucially, culturally learned skills vary from place to place. In the human family many cultures, underappreciated, have been lost. Culture in the other-than-human world has been almost entirely missed.

We are just recognising that in many species, survival skills must be learned from elders who learned from their elders. Until now, culture has remained a largely hidden, unrecognised layer of wild lives. Yet for many species culture is both crucial and fragile. Long before a population declines to numbers low enough to seem threatened with extinction, their special cultural knowledge, earned and passed down over long generations, begins disappearing. Recovery of lost populations then becomes much more difficult than bringing in a few individuals and turning them loose.

Many young birds learn much by observing their parents, and parrots probably need to learn more than most. Survival of released individuals is severely undermined if there are no free-living elder role models. Trying to restore parrot populations by captive breeding is not as easy as training young or orphaned creatures to recognise what is food while theyre in the safety of a cage then simply opening the door. In a cage, Williams says, you cant train them to know where, when and how to find that food, or about trees with good nest sites. Parents would normally have done exactly that.

A generational break in cultural traditions hampered attempts to reintroduce thick-billed parrots to parts of south-west America, where theyd been wiped out. Conservation workers could not teach the captive-raised parrots to search for and find their traditional wild foods, skills they would have learned from parents.

Landscapes, always complex, are under accelerated change. Culture enables adaptation far faster than genes alone can navigate hairpin turns in time. In some places, pigeons and sparrows have learned to use motion-sensors to get inside enclosed shopping malls and forage for crumbs. Crows have in some locales learned to drop nuts on the road for cars to crack. In at least one area they do this at intersections, so they can safely walk out and collect their cracked prizes when the light turns red and the cars stop. Theyve developed answers to the new question: How can we survive here, in this never-before world?

Because the answers are local, and learned from elders, wild cultures can be lost faster than genetic diversity. When populations plummet, traditions that helped animals survive and adapt to a place begin to vanish.

In a scientific article on the vocabulary of larks living in north Africa and Spain titled, Erosion of animal cultures in fragmented landscapes, researchers reported that as human development shrinks habitats into patches, isolation is associated with impoverishment. They write: Song repertoires pass through a cultural bottleneck and significantly decline in variety.

Unfortunately, isolated larks are not an isolated case. Researchers studying South Americas orange-billed sparrow found that sparrow song complexity the number of syllables per song and song length deteriorated as humans continued whittling their forests into fragments. When a scientist replayed 24-year-old recordings of singing male white-crowned sparrows at the same location shed recorded them, they elicited half the responses they had when first recorded. The birds responses show that changes in the dialect lead to changes in listener preference, a bit analogous to pop music. And as with humans, preferences can affect whether a particular bird will be accepted as a mate. White-crowned sparrows singing a local dialect become fathers of more offspring than do singers of unfamiliar dialects, indicating females prefer a familiar tune.

Im not just talking about a few songs. Survival of numerous species depends on cultural adaptation. How many? Were just beginning to ask such questions. But the preliminary answers indicate surprising and widespread ways that animals survive by cultural learning. Regionally different vocalisations are sometimes called song traditions but the more commonly used word is dialects. More than a hundred studies have been published on dialects in birds. And its not just birds but a wide array of animals Including some fish.

Cod particularly, said Steve Simpson of the University of Exeter, have very elaborate calls compared with many fish. You can easily hear differences in recorded calls of American and European Atlantic cod. This species is highly vocal with traditional breeding grounds established over hundreds or even thousands of years. Many fish follow elders to feeding, resting and breeding areas. In experiments, introduced outsiders who learned such preferred locales by following elders continued to use these traditional routes after all the original fish from whom they learned were gone.

Cultural survival skills erode as habitats shrink. Maintaining genetic diversity is not enough. Weve become accustomed to a perilous satisfaction with precariously minimal populations that not only risk genetic viability of populations but almost guarantee losing local cultural knowledge by which populations have lived and survived.

In all free-living parrots that have been studied, nestlings develop individually unique calls, learned from their parents. Researchers have described this as an intriguing parallel with human parents naming infants. Indeed, these vocal identities help individuals distinguish neighbours, mates, sexes and individuals; the same functions that human names serve.

Williams tells me that when he studied Amazon parrots, he could hear differences between them saying, essentially, Lets go, Im here, where are you? and Darling, I just brought breakfast. Researchers who develop really good ears for parrot vocalisation and use technology to study recordings show that parrot noise is more organised and meaningful than it sounds to beginners like me. In a study of budgerigars, for instance, birds who were unfamiliar with each other were placed together. Groups of unfamiliar females took a few weeks for their calls to converge and sound similar. Males copied the calls of females. Black-capped chickadees flock members calls converge, so they can distinguish members of their own flock from those of other flocks. The fact that this happens, and that it takes weeks, suggests that free-living groups must normally be stable, that groups have their own identity, and that the members identify with their group.

Group identity, we see repeatedly, is not exclusively human. Sperm whales learn and announce their group identity. Young fruit bats learn the dialects of the crowds theyre in. Ravens know whos in, whos out. Too many animals to list know what group, troop, family or pack they belong with. In Brazil, some dolphins drive fish toward fishermens nets for a share of the catch. Other dolphins dont. The ones who do, sound different from the ones who dont. Various dolphin groups who specialise in a food-getting technique wont socialise with other groups who use different techniques. And orca whales, the most socially complex non-humans, have layered societies of pods, clans and communities, with community members all knowing the members of all their constituent pods, but each community scrupulously avoiding contact with members of another community. All this social organisation is learned from elders.

Elders appear important for social learning of migratory routes. Various storks, vultures, eagles and hawks all depend on following the cues of elders to locate strategic migration flyways or important stopover sites. These could be called their migration cultures. Famously, conservationists have raised young cranes, geese and swans to follow microlight aircraft as a surrogate parent on first migrations. Without such enculturation, they would not have known where to go. The young birds absorbed knowledge of routes, then used them in later seasons on their own self-guided migrations. Four thousand species of birds migrate, so Andrew Whiten of the University of St Andrews in Scotland speculates that following experienced birds may be an underappreciated but very significant realm of cultural transmission.

When you look at free-living animals, you dont usually see culture. Culture makes itself visible when it gets disrupted. Then we see that the road back to reestablishing cultures the answers to the questions of how we live in this place is difficult, often fatal.

Young mammals too moose, bison, deer, antelope, wild sheep, ibex and many others learn crucial migration routes and destinations from elder keepers of traditional knowledge. Conservationists have recently reintroduced large mammals in a few areas where theyve been wiped out, but because animals released into unfamiliar landscapes dont know where food is, where dangers lurk, or where to go in changing seasons, many translocations have failed.

Williams describes his procedure with the macaws as very much a slow release. First his team trains the birds to use a feeder. With that safety net, they can explore the forest, gain local knowledge, begin dispersing and using wild foods.

Some rescue programmes declare success if a released animal survives one year. A year is meaningless for a bird like a macaw that doesnt mature until its eight years old, says Williams.

I ask what theyre doing for those eight long years.

Social learning, Williams replies immediately. Working out whos who, how to interact, like kids in school.

To gain access to the future, to mate and to raise young, the birds Williams is releasing must enter into the culture of their kind. But from whom will they learn, if no one is out there? At the very least they must be socially oriented to one another. Ex-pets are the worst candidates for release; they dont interact appropriately with other macaws, and they want to hang around near humans.

To assess the social abilities of 13 scarlet macaws who were scheduled for release, Williams and his crew documented how much time they spent close to another bird, how often they initiated aggression, things like that. When the bird scoring lowest for social skills was released, he flew out the door and was never seen again. The next-to-lowest didnt adapt to the free-living life and had to be retrieved. The third-lowest social scorer remained at liberty but stayed alone a lot. The rest did well.

All of the above adds up to this: a species isnt just one big jar of jellybeans of the same colour. Its different smaller jars with differing hues in different places. From region to region, genetics can vary. And cultural traditions can differ. Different populations might use different tools, different migration routes, different ways of calling, courting and being understood. All populations have their answers to the question of how to live where they live.

Sometimes a group will be foraging in a tree, Williams says. A pair will fly overhead on a straight path. Someone will make a contact call, and the flying birds will loop around and land with the callers. They seem to have their friends. Bottom line, said Williams, there is much going on in the social and cultural lives of his macaws and other species, much that they understand but we dont. We have a lot of questions. The answers must lurk, somewhere, in their minds.

As land, weather and climate change, some aspects of cultural knowledge will be the tickets necessary for boarding the future. Others will die out. Across the range of chimpanzees, cultures vary greatly, as do habitats. All populations but one use stick tools. Some use simple probes, others fashion multi-stick toolsets. Only one population makes pointed daggers for hunting small nocturnal primates called bush-babies hiding in tree holes. Only the westernmost chimpanzees crack nuts with stones.

As researchers have noted, distinctive tool-using traditions at particular sites are defining features of unique chimpanzee cultures. Whiten wrote: Chimpanzee communities resemble human cultures in possessing suites of local traditions that uniquely identify them A complex social inheritance system that complements the genetic picture.

Some chimpanzee populations have learned to track the progress of dozens of specific trees ripening in their dense forests. Others live in open semi-savannah. Some are more aggressively male-dominated, some populations more egalitarian. Some almost never see people; some live in sight of human settlements and have learned to crop-raid at night. For a long, long time chimpanzees have been works in progress. Weve learned, writes Craig Stanford, not to speak of The Chimpanzee. Chimpanzees vary and chimpanzee culture is variable at every level.

Its not just the loss of populations of chimps that worries me, Cat Hobaiter emphasised when I spent several weeks with her studying chimpanzees in Uganda. I find terrifying the possibility of losing each populations unique culture. Thats permanent.

Diversity in cultural pools perhaps more crucially than in gene pools will make species survival more likely. If pressures cause regional populations to blink out, a species odds of persisting dim.

Williams goal is to re-establish macaws where they range no longer, in hopes that they, and their forests, will recover. (Most of the central American forests that macaws need have been felled and burned, largely so fast-food burger chains can sell cheap beef.) It often takes a couple of generations for human immigrant families to learn how to function effectively in their new culture; it may take two or three generations before an introduced population of macaws succeeds. In other words, macaws are born to be wild. But becoming wild requires an education.

So whats at stake is not just numbers. Whats at stake is: ways of knowing how to be in the world. Culture isnt just a boutique concern. Cultural knowledge is what allows many populations to survive. Keeping the knowledge of how to live in a habitat can be almost as important to the persistence of a species as keeping the habitat; both are needed. Cultural diversity itself is a source of resilience and adaptability to change. And change is accelerating.

This is an edited extract from Becoming Wild: How Animals Learn to be Animals by Carl Safina, which published in the UK by Oneworld on 9 April and in the US by Henry Holt and Co on 14 April

Continue reading here:

The secret call of the wild: how animals teach each other to survive - The Guardian

Yann Joly, Research Director of the Centre of Genomics and Policy

Research Director of the Centre of Genomics and Policy and Associate Professor at the Department of Human Genetics, Yann Joly is a Lawyer Emeritus from the Quebec Bar and a Fellow of the Canadian Academy of Health Sciences. He is currently a member of the Quebec task force on theCOVID-19 Biobank.

Last week, Joly and his collaborators from 16 countries announced the establishment of the international Genetic Discrimination Observatory (GDO). A world first, the GDO is an online platform committed to preventing the misuse of a patients genetic information. This is particularly important within the current context of the COVID-19 pandemic when researchers are collecting samples and data from patients in order to better understand this new disease and develop effective vaccines or therapeutics.

In this Q&A, Joly gives readers more information on genetic discrimination and what is being done to combat it.

Genetic discrimination (GD) means treating people differently from the rest of the population or unfairly profiling them based on actual or presumed genomic and other predictive medical data. The genetic information contained in an individuals DNA can uniquely identify or provide some information about a person, including future probabilities that this individual will develop diseases. Other predictive health information, such as biomarkers, can also be used to discriminate and should also be considered under the GD heading.

This information can be of interest to third parties like insurers, employers, or government officials. Like sexual, ethnic or disability-based discrimination, genetic discrimination is a source of exclusion and can limit the social and professional opportunities of a person thus becoming a source of psychological distress.

There are documented cases of GD reported in studies carried out in a limited number of countries based on predictive test results and family history for a handful of severe single-gene conditions in the context of life insurance or employment. The available evidence is fragmentary, and the methodology used in many studies is inconsistent.

The Genetic Non-Discrimination Act (hereinafter S-201) was passed in April 2017 and is currently applicable in Canada. While it does not solve all the challenges posed by genetic discrimination, it is an important first step. The Act generally makes it a criminal offense to require a person to undergo a genetic test or to report the results as a condition precedent to the provision of goods and services. However, the Quebec Court of Appeal recently declared that the core elements of S-201 were not constitutionally valid.

This decision was appealed to the Supreme Court of Canada and we are currently waiting for their decision on the matter. In the meantime, S-201 continue to be applied. If the Supreme Court is of a similar opinion to that of the Court of Appeal, it could be invalidated.

In addition to the protection provided by S-201, Canadian privacy laws would fully apply to genetic data, which is considered personal information.

Genetic information is increasingly shared across national borders or transcending them, thus limiting the effectiveness of protections built solely around national approaches. Strictly legal solutions, because they tend to be static, are also challenged to keep pace with rapidly evolving science such as genetics.

At its core discrimination is a social phenomenon that needs to be addressed collaboratively and internationally by all stakeholders. The GDO will provide the platform to undertake this important work, which will include documenting instances of genetic discrimination, identifying most effective preventing measures and conveying information, tools and good practices to all stakeholders including the public.

COVID-19 presents Quebecers with an unprecedented health threat that requires us to stand together as a society and take action to protect one another and help find medical solutions to the disease. The COVID-19 Biobank provides us a unique opportunity to learn more about the biological foundations of the disease, individuals at risk and preventive solutions.

The risk of discrimination associated with providing a biological sample and medical information to the Biobank is very small. The data provided is research information that is not clinically validated and should be of no interest to most third parties. Moreover, the collected information is coded, and protected by confidentiality laws and robust security measures. Furthermore, data access will be subject to ethics approval and in some cases controlled access measures.

Here is the original post:

Yann Joly on the fight against genetic discrimination - McGill Reporter

Humanity really has only two options to confront the coronavirus pandemic currently sweeping the planet. The first is to mount a rolling program of lockdowns and other drastic social distancing strategies to restrain the pace of the virus epidemic, with a view to gradually building up natural herd immunity among the human population.

That strategy, especially if combined with successful anti-viral drug treatments and a massively upscaled testing effort, should give some relief. But it would come at the likely cost of many millions of deaths and incalculable worldwide economic damage, hitting especially hard in countries with little resilience and limited healthcare infrastructure.

The second approach is to develop a vaccine, and to do so as rapidly as possible. A fully effective vaccine would not just tame COVID-19 but possibly eradicate it altogether as the world successfully did with smallpox and is on the verge of doing with polio (both also viral diseases).

These two approaches will most likely be concurrent: the first will buy us time, while the second provides an exit strategy from a constant pattern of repeating lockdowns and travel restrictions that could otherwise go on for years.

With the current total of confirmed cases rapidly closing in on one million worldwide, the true picture is most likely that many tens of millions of people have already caught COVID-19. Humanitys most desperate challenge, therefore, is to find an effective vaccine.

Fortunately, science is already stepping up. History was made on March 16, when the first clinical trial volunteer was injected with an investigational vaccine for coronavirus at the Kaiser Permanente Washington Health Research Institute in Seattle.

The volunteer was mother-of-two Jennifer Haller, a 43-year-old Seattle resident who told National Public Radio that she wanted to do something because theres so many Americans that dont have the same privileges that Ive been given.

The vaccination was produced by Moderna, with the first batch being delivered to the US National Institutes of Health a remarkable 42 days after the viral genome was first sequenced in China.

This Phase 1 trial does not yet test the efficacy of the vaccine against COVID-19. Carried out over six weeks among a group of 45 healthy adult volunteers aged between 18 and 55, it will test the basic safety of the proposed vaccine and its ability to stimulate an immune response in the human body.

Although the Phase 1 trial will continue with the Seattle-area recruits being monitored for a whole year, the urgency of the global situation means that the collaborators will likely rush to Phase 2 at the same time, testing the ability of the vaccine to prevent infection by the novel coronavirus SARS-CoV-2 that causes COVID-19.

The Moderna vaccine trial is a world first not just for the particular disease target but because it is one of a whole new potential class of vaccines that employ messenger RNA (mRNA) to program human cells to produce the viral proteins that trigger an immune response, rather than injecting proteins or viral particles directly, as have most previous vaccines.

This natural role of mRNA is why Modernas approach is so quick. Normal vaccines have to be produced from actual viruses, which are grown within chicken eggs and then refined into sufficient quantities to be directly injected once weakened or killed into the human body. This takes months, at a minimum, and is difficult to scale quickly.

For the mRNA approach, all that was needed was the correct viral genetic sequence, which in the case of SARS-CoV-2 encodes for the spike proteins that enable the virus to gain entry into human respiratory cells. This genetic sequence for the viral protein can then be encoded into mRNA synthetically generated in a lab a rapid process that is easy to scale.

Thats the good news. The bad news is that the mRNA approach, while undoubtedly quick and versatile, is so new that it has yet to be fully proven in any vaccine in either humans or animals. Some tests have shown efficacy against rabies, for example, but others have shown little lasting immune response.

The mRNA approach is therefore a moon-shot rather than a marathon. Even so, Moderna is optimistic enough to already be making plans to produce millions of doses intended for health workers initially as early as this fall.

Other companies and partnerships are also racing to develop a vaccine using the same mRNA approach. One of these, the German firm CureVac, generated so much interest that President Trump reportedly tried to acquire it in order to ensure any potential vaccine would be available to Americans first.

Like Moderna, CureVacs efforts are supported financially by CEPI the international Coalition for Epidemic Preparedness Innovations, which has raised over $700 million from governments around the world and philanthropic foundations like the Bill & Melinda Gates Foundation (which also supports the Cornell Alliance for Science) and Wellcome.

While Moderna has been able to restart vaccine projects originally intended for MERS and SARS, CureVac has already achieved some success with an mRNA vaccine against rabies virus in humans. In a Phase 1 trial doses as low as a millionth of a gram of mRNA vaccine were sufficient to fully protect humans against rabies, it reported in January.

Such small doses offer major promise for immunizing huge numbers of people if CureVac is able to achieve the same success with SARS-CoV-2 as it has with rabies and move rapidly into Phase 2 trials to further demonstrate real efficacy.

Also in Germany, BioNTech and Pfizer are racing to shift their mRNA vaccine work from influenza to SARS-CoV-2, and are aiming to start clinical trials as soon as April. As part of a broader collaboration, BioNTech has already demonstrated that an mRNA vaccine protected mice and non-human primates against Zika virus, raising hopes for similar effectiveness against COVID-19.

RNAs double-stranded cousin, DNA, is also being deployed in a novel but equally promising vaccine system against the coronavirus. The approach is related, but rather than injecting mRNA directly into cells so that it can produce viral proteins, DNA is inserted, which in turn produces mRNA inside cells to do the same job.

This DNA is not intended to integrate into the genome of the target cell in humans indeed if this happens, damaging mutations might occur. Instead, DNA is formed into circular plasmids which operate separately to the integral genetic material inside a cells nucleus. Like genomic DNA however, these plasmids are read and transcribed via mRNA into viral proteins which can then prime the bodys immune system against a later invasion by the real virus.

The US-based Inovio Pharmaceuticals announced on 12 March that it had received a grant of $5 million from the Bill & Melinda Gates Foundation to accelerate the testing of a DNA vaccine for COVID-19, with a view to starting Phase 1 clinical trials in April.

Inovio has another advantage: its DNA vaccine INO-4700 was the only vaccine candidate against MERS to progress to Phase 2 trials demonstrating, at least initially, the potential feasibility of the DNA approach. The US Department of Defense with an eye to protecting its military personnel all over the world against COVID-19 has pumped another $11.9 million into INO-4800. The company has also demonstrated protection in early trials using its DNA vaccine against Chikungunya, Zika and influenza viruses.

CEPI is not putting all its eggs in one basket, however. As well as DNA and RNA systems, another promising approach for a COVID-19 vaccine is to use a genetically engineered measles vaccine a strategy supported by a $5 million CEPI grant split between collaborating institutions Themis in Vienna, Institut Pasteur in France and the University of Pittsburghs Center for Vaccine Research.

This takes the live attenuated measles virus vaccine a vaccine with a long history of safe use, having been used to immunize billions of children over the last 40 years and uses reverse genetics technology to insert new genes coding for proteins expressed by other viruses. These then induce an immune response against the new virus whose genetic material has been introduced.

The research team aims to have a COVID-19 candidate vaccine ready for animal testing as soon as April, with wider tests in human volunteers by the end of the year.

Measles virus is not the only candidate for the vector approach. Chinese scientists have reported that they are about to proceed to Phase I human trials with a vaccine candidate starting at the pandemics epicenter in Wuhan. The scientists have genetically engineered a replication-defective adenovirus type 5 (Ad5) as a vector to express the SARS-CoV-2 spike protein, with the resulting vaccine candidate named Ad5-nCoV.

This is perhaps the easiest approach, as all that has to happen is for the engineered harmless adenovirus to infect patients in order to trigger the production of antibodies which should be effective against invading novel coronavirus too. The Chinese company CanSion Biologics has successfully demonstrated this approach with another fully completed vaccine against Ebola, Ad5-EBOV, which is already on the market in China.

A more tried-and-tested approach already widely used to produce flu vaccines is to grow viral proteins directly: these are then injected as a vaccine into human patients so that the immune system is already primed against the real pathogen when it attempts to infect the body. Usually chicken eggs are used, but to speed things up insect cell lines are becoming the preferred option for the coronavirus pandemic.

Here genetics is again an important component: the company Novavax uses a baculovirus vector to genetically engineer an insect cell line originally isolated decades ago from the ovaries of the fall armyworm. The baculovirus transports genes into the insect cells, which program them to manufacture viral proteins that are correctly folded and biologically active, more reliably enabling the human immune system to produce antibodies against them.

According to Novavax, its resulting recombinant protein nanoparticles then self-assemble into a structure that approximates the actual virus, helping enhance the immune response. It claims to have already tested this system in RSV virus, a recalcitrant pathogen that has so far resisted attempts at a vaccine. This approach looks promising enough that CEPI has pumped $4 million in so far with a view to launching Phase I trials by late spring 2020.

In a similar way, the company Sanofi is taking a snippet of genetic code from SARS-CoV-2 and splicing it also via baculovirus into insect cell lines. Its advantage, made in a pitch to the US government that resulted in a big cash injection, is that it already has an FDA-approved facility that could make 600 million doses a year of any resulting vaccine.

Plants can also be engineered to produce viral proteins. The company Medicago is working with genetically modified tobacco plants with this aim in mind. To speed things up, instead of adding new genes to the nucleus of cells and regenerating entire plants from these single cells (as happens with conventional plant genetic engineering), it uses the Agrobacterium vector in a vacuum to transfer recombinant DNA directly into the nucleus of fully-grown leaf cells. This DNA enables the production of the desired viral proteins without ever being integrated into the genome, enabling proteins to be harvested from transformed leaves within a matter of days.

Using this system, Medicago claims to have produced a virus-like particle of the coronavirus within just 20 daysof the SARS-CoV-2 genetic sequence becoming available. The government of Canada quickly put millions of dollars behind the effort as a result.

Astonishingly, given that the coronavirus pandemic is now threatening to devastate societies and economies around the planet on a scale second only to a world war, this effort is still short of cash. CEPI has issued an urgent call for funding, seeking to raise $2 billion: it says just $375 billion by the end of March would enable four-to-six vaccine candidates to move rapidly towards phase 2/3 trials.

Scientists are also hoping desperately that SARS-CoV-2 does not rapidly mutate as influenza viruses tend to do, which would likely reduce the effectiveness of any single vaccine. So far, according to researchers studying 1,000 samples of the virus from around the world, this seems not to be the case.

This means that the race to find a vaccine, and to do so in sufficient time to salvage the situation before the world tips into an economic depression and millions of people die, has a decent chance of success and that any successful vaccine would likely confer lasting immunity.

Meanwhile, all of humanity is waiting. And if the scientists do succeed in this urgent challenge, it will very likely be due to modern genetics. Though genetic engineering was once a dirty word, it now could literally help save the world.

This article originally ran at theCornell Alliance for Scienceand has been republished here with permission. Follow the Alliance for Science on Twitter @ScienceAlly. Follow Mark Lynas on Twitter @mark_lynas

The rest is here:

Science to the rescue? How modern genetics could help save the world from coronavirus - Genetic Literacy Project

Haaretz.com

***

Researchers have recovered the oldest human genetic information to date from two prehistoric teeth, one 1.77 million old and the other 800,000 years in age. The remains are so old they belong to a time that precedes the evolution of modern humans, i.e. Homo sapiens, so technically they are human only in the sense that they belong to some of our predecessors in the Homo evolutionary tree.The older of the two teeth was found in Dmanisi cave in Georgia and belonged to Homo erectus, the first hominin group known to have left Africa and spread throughout Eurasia.The second tooth was unearthed at a prehistoric site in Spains Atapuerca Mountains and belonged to a Homo antecessor, an enigmatic early human with a penchant for cannibalism whose evolutionary relationship to us has been the subject of much debate.The new research published Wednesday in Nature and led by scientists from the University of Copenhagen has provided a partial answer to that question, revealing that Homo antecessor was not a direct ancestor of Homo sapiens, as had been surmised by some.Both the analyzed samples precede by hundreds of thousands of years what was until now the oldest sequenced human genome, the 430,000-year-old DNA extracted from the remains of an early Neanderthal that was also found at Atapuerca.To achieve this huge leap forward or actually, backwards in the study of evolutionary genetics, the scientists used a new method that doesnt reconstruct ancient DNA but sequences proteins, in this case those found in the dental enamel, the hardest and most durable part of the human body.The Gran Dolina site in the Atapuerca Mountains , the only source of Homo antecessor boneAriel DavidSince proteins are built by our cells based on instructions from our nuclear DNA, the amino acid chains that form them represent a sort of mirror image of the nucleotides that form constitute our genetic code, explains Dr. Frido Welker, a molecular anthropologist at the University of Copenhagen.Breaking news and analyses in your inboxThank you for signing up.Weve got more newsletters we think youll find interesting.Click hereOops. Something went wrong.Please try again later.Try againThank you,The email address you have provided is already registered.CloseJust like DNA sequences, these protein sequences will be slightly different between different people, populations and species in a manner that is determined by their evolution, Welker tells Haaretz. So by comparing sequences from different prehistoric and modern populations, experts can approximate how closely related these ancient groups are to each other.The advantage of hunting for proteins instead of DNA is that the latter molecule tends to degrade faster, says Enrico Cappellini a professor at the University of Copenhagen and one the lead authors on the Nature study.Until now, the oldest animal DNA sequenced has been that of a 700,000-year-old horse and that was only because its remains had been preserved by Canadas permafrost. By using palaeoproteomics (the study of ancient proteins), the same Danish team has published protein sequences from a 1.77-million-year-old rhino found at Dmanisi, as well as a 1.9-million-year old Gigantopithecus, an extinct great ape from China.Of course, even this new approach has limits. So if you have nightmares about being chased by a velociraptor in a Jurassic-Park-like scenario, then know we are still very far away from sequencing the proteins let alone the DNA of dinosaurs who went extinct 65 million years ago.In fact, even the 1.77-million-year old protein sequence belonging to the Homo erectus from Dmanisi was too short and damaged to be of much use to the authors of the new study, Welker says. It still stands as the oldest genetic information we have gathered on a human ancestor, but it cannot tell us anything about the evolutionary link between erectus and sapiens.Digital reconstruction of specimen ATD6-69 from the Homo antecessor collection. Computerized microtomography techniques were used to perform this reconstructionProf. Laura Martn-FrancsClose, but no ancestorThe study of the Homo antecessor tooth was, on the other hand, much more revealing.Remains of this hominin have been found only at that one site in Spains Atapuerca Mountains, though some prehistoric stone tools unearthed in France and Britain suggest it may have been present there too between 1.2 and 0.8 million years ago. Very little is known about their behavior, apart from the fact that some of their bones were skillfully butchered, which has been interpreted as the earliest evidence of human cannibalism.Still, some scholars have theorized that antecessor may have played an outsize role in our evolution.As hinted by its Latin name, which means predecessor or ancestor, the hypothesis is that this elusive hominin was the last common ancestor of Homo sapiens, Neanderthal and Denisovan, the main hominin groups that inhabited the Earth over the last half-million years. The theory is based on the fact that antecessor shares some features with later hominins, especially a relatively modern-looking face. Also, the time span of antecessors existence fits well with other studies suggesting that the lineages that eventually led to the evolution of Neanderthals, sapiens and Denisovans split off some time before 750,000 years ago.But the Nature study, titled The dental proteome of Homo antecessor, does not support this theory. Once the recovered protein sequences were compared to those of other hominins, it became apparent that antecessor could only be a sister group of that mysterious common ancestor we share with Neanderthals and Denisovans.The Gran Dolina site in the Atapuerca Mountains , the only source of Homo antecessor bonesAriel DavidThe caveat is that it is difficult to establish how closely related they were to the common ancestor, Welker tells Haaretz. In other words, we are relatives, but antecessor is not on the same branch as us in the evolutionary tree.Personally, I am glad that our ancestors did not diverge from a group of cannibals, jokes Prof. Israel Hershkovitz, a physical anthropologist from Tel Aviv University.The recovery of the protein sequences from the erectus and antecessor teeth is an impressive technical feat, says Hershkovitz, who did not take part in the study.Palaeoproteomics allows us to gain insights about earlier times than by using DNA, but it is also a more limited tool that, as the authors stated, can only give us a best guess as to the placement of Homo antecessor in relation to later hominin groups, he cautions.The studys conclusion that antecessor was a parallel group to one of our distant ancestors does contribute to the growing evidence suggesting that human evolution is anything but a straight line in which one type of hominin evolves into the next one, Welker notes. Research over the last years has shown that our evolutionary history resembles more a tangled bush in which different populations evolved in parallel, coexisted and mixed continuously.Many questions remain unanswered, such as the identity of that missing link between us and our closest evolutionary cousins, the Neanderthals and Denisovans, Welker says. But the newfound ability to glean at least some genetic material from hominin remains that are millions of years old does hint that maybe we will be able to crack that mystery soon, as well as other open questions about our distant origins.The Sima de los Huesos, or Bone pit in the Atapuerca Mountains, where dozens of Neanderthal bodies were foundAriel DavidThe Sima de los Huesos, or Bone pit in the Atapuerca Mountains, where dozens of Neanderthal bodies were foundAriel David

Continue reading here:

Oldest human genetic data gleaned from 1.8-million-year-old tooth Haaretz - News Collective

Humanity really has only two options to confront the coronavirus pandemic currently sweeping the planet. The first is to mount a rolling program of lockdowns and other drastic social distancing strategies to restrain the pace of the virus epidemic, with a view to gradually building up natural herd immunity among the human population.

That strategy, especially if combined with successful anti-viral drug treatments and a massively upscaled testing effort, should give some relief. But it would come at the likely cost of many millions of deaths and incalculable worldwide economic damage, hitting especially hard in countries with little resilience and limited healthcare infrastructure.

The second approach is to develop a vaccine, and to do so as rapidly as possible. A fully effective vaccine would not just tame COVID-19 but possibly eradicate it altogether as the world successfully did with smallpox and is on the verge of doing with polio (both also viral diseases).

These two approaches will most likely be concurrent: the first will buy us time, while the second provides an exit strategy from a constant pattern of repeating lockdowns and travel restrictions that could otherwise go on for years.

With the current total of confirmed cases rapidly closing in on one million worldwide, the true picture is most likely that many tens of millions of people have already caught COVID-19. Humanitys most desperate challenge, therefore, is to find an effective vaccine.

Fortunately, science is already stepping up. History was made on March 16, when the first clinical trial volunteer was injected with an investigational vaccine for coronavirus at the Kaiser Permanente Washington Health Research Institute in Seattle.

The volunteer was mother-of-two Jennifer Haller, a 43-year-old Seattle resident who told National Public Radio that she wanted to do something because theres so many Americans that dont have the same privileges that Ive been given.

The vaccination was produced by Moderna, with the first batch being delivered to the US National Institutes of Health a remarkable 42 days after the viral genome was first sequenced in China.

This Phase 1 trial does not yet test the efficacy of the vaccine against COVID-19. Carried out over six weeks among a group of 45 healthy adult volunteers aged between 18 and 55, it will test the basic safety of the proposed vaccine and its ability to stimulate an immune response in the human body.

Although the Phase 1 trial will continue with the Seattle-area recruits being monitored for a whole year, the urgency of the global situation means that the collaborators will likely rush to Phase 2 at the same time, testing the ability of the vaccine to prevent infection by the novel coronavirus SARS-CoV-2 that causes COVID-19.

The Moderna vaccine trial is a world first not just for the particular disease target but because it is one of a whole new potential class of vaccines that employ messenger RNA (mRNA) to program human cells to produce the viral proteins that trigger an immune response, rather than injecting proteins or viral particles directly, as have most previous vaccines.

This natural role of mRNA is why Modernas approach is so quick. Normal vaccines have to be produced from actual viruses, which are grown within chicken eggs and then refined into sufficient quantities to be directly injected once weakened or killed into the human body. This takes months, at a minimum, and is difficult to scale quickly.

For the mRNA approach, all that was needed was the correct viral genetic sequence, which in the case of SARS-CoV-2 encodes for the spike proteins that enable the virus to gain entry into human respiratory cells. This genetic sequence for the viral protein can then be encoded into mRNA synthetically generated in a lab a rapid process that is easy to scale.

Thats the good news. The bad news is that the mRNA approach, while undoubtedly quick and versatile, is so new that it has yet to be fully proven in any vaccine in either humans or animals. Some tests have shown efficacy against rabies, for example, but others have shown little lasting immune response.

The mRNA approach is therefore a moon-shot rather than a marathon. Even so, Moderna is optimistic enough to already be making plans to produce millions of doses intended for health workers initially as early as this fall.

Other companies and partnerships are also racing to develop a vaccine using the same mRNA approach. One of these, the German firm CureVac, generated so much interest that President Trump reportedly tried to acquire it in order to ensure any potential vaccine would be available to Americans first.

Like Moderna, CureVacs efforts are supported financially by CEPI the international Coalition for Epidemic Preparedness Innovations, which has raised over $700 million from governments around the world and philanthropic foundations like the Bill & Melinda Gates Foundation (which also supports the Cornell Alliance for Science) and Wellcome.

While Moderna has been able to restart vaccine projects originally intended for MERS and SARS, CureVac has already achieved some success with an mRNA vaccine against rabies virus in humans. In a Phase 1 trial doses as low as a millionth of a gram of mRNA vaccine were sufficient to fully protect humans against rabies, it reported in January.

Such small doses offer major promise for immunizing huge numbers of people if CureVac is able to achieve the same success with SARS-CoV-2 as it has with rabies and move rapidly into Phase 2 trials to further demonstrate real efficacy.

Also in Germany, BioNTech and Pfizer are racing to shift their mRNA vaccine work from influenza to SARS-CoV-2, and are aiming to start clinical trials as soon as April. As part of a broader collaboration, BioNTech has already demonstrated that an mRNA vaccine protected mice and non-human primates against Zika virus, raising hopes for similar effectiveness against COVID-19.

RNAs double-stranded cousin, DNA, is also being deployed in a novel but equally promising vaccine system against the coronavirus. The approach is related, but rather than injecting mRNA directly into cells so that it can produce viral proteins, DNA is inserted, which in turn produces mRNA inside cells to do the same job.

This DNA is not intended to integrate into the genome of the target cell in humans indeed if this happens, damaging mutations might occur. Instead, DNA is formed into circular plasmids which operate separately to the integral genetic material inside a cells nucleus. Like genomic DNA however, these plasmids are read and transcribed via mRNA into viral proteins which can then prime the bodys immune system against a later invasion by the real virus.

The US-based Inovio Pharmaceuticals announced on 12 March that it had received a grant of $5 million from the Bill & Melinda Gates Foundation to accelerate the testing of a DNA vaccine for COVID-19, with a view to starting Phase 1 clinical trials in April.

Inovio has another advantage: its DNA vaccine INO-4700 was the only vaccine candidate against MERS to progress to Phase 2 trials demonstrating, at least initially, the potential feasibility of the DNA approach. The US Department of Defense with an eye to protecting its military personnel all over the world against COVID-19 has pumped another $11.9 million into INO-4800. The company has also demonstrated protection in early trials using its DNA vaccine against Chikungunya, Zika and influenza viruses.

CEPI is not putting all its eggs in one basket, however. As well as DNA and RNA systems, another promising approach for a COVID-19 vaccine is to use a genetically engineered measles vaccine a strategy supported by a $5 million CEPI grant split between collaborating institutions Themis in Vienna, Institut Pasteur in France and the University of Pittsburghs Center for Vaccine Research.

This takes the live attenuated measles virus vaccine a vaccine with a long history of safe use, having been used to immunize billions of children over the last 40 years and uses reverse genetics technology to insert new genes coding for proteins expressed by other viruses. These then induce an immune response against the new virus whose genetic material has been introduced.

The research team aims to have a COVID-19 candidate vaccine ready for animal testing as soon as April, with wider tests in human volunteers by the end of the year.

Measles virus is not the only candidate for the vector approach. Chinese scientists have reported that they are about to proceed to Phase I human trials with a vaccine candidate starting at the pandemics epicenter in Wuhan. The scientists have genetically engineered a replication-defective adenovirus type 5 (Ad5) as a vector to express the SARS-CoV-2 spike protein, with the resulting vaccine candidate named Ad5-nCoV.

This is perhaps the easiest approach, as all that has to happen is for the engineered harmless adenovirus to infect patients in order to trigger the production of antibodies which should be effective against invading novel coronavirus too. The Chinese company CanSion Biologics has successfully demonstrated this approach with another fully completed vaccine against Ebola, Ad5-EBOV, which is already on the market in China.

A more tried-and-tested approach already widely used to produce flu vaccines is to grow viral proteins directly: these are then injected as a vaccine into human patients so that the immune system is already primed against the real pathogen when it attempts to infect the body. Usually chicken eggs are used, but to speed things up insect cell lines are becoming the preferred option for the coronavirus pandemic.

Here genetics is again an important component: the company Novavax uses a baculovirus vector to genetically engineer an insect cell line originally isolated decades ago from the ovaries of the fall armyworm. The baculovirus transports genes into the insect cells, which program them to manufacture viral proteins that are correctly folded and biologically active, more reliably enabling the human immune system to produce antibodies against them.

According to Novavax, its resulting recombinant protein nanoparticles then self-assemble into a structure that approximates the actual virus, helping enhance the immune response. It claims to have already tested this system in RSV virus, a recalcitrant pathogen that has so far resisted attempts at a vaccine. This approach looks promising enough that CEPI has pumped $4 million in so far with a view to launching Phase I trials by late spring 2020.

In a similar way, the company Sanofi is taking a snippet of genetic code from SARS-CoV-2 and splicing it also via baculovirus into insect cell lines. Its advantage, made in a pitch to the US government that resulted in a big cash injection, is that it already has an FDA-approved facility that could make 600 million doses a year of any resulting vaccine.

Plants can also be engineered to produce viral proteins. The company Medicago is working with genetically modified tobacco plants with this aim in mind. To speed things up, instead of adding new genes to the nucleus of cells and regenerating entire plants from these single cells (as happens with conventional plant genetic engineering), it uses the Agrobacterium vector in a vacuum to transfer recombinant DNA directly into the nucleus of fully-grown leaf cells. This DNA enables the production of the desired viral proteins without ever being integrated into the genome, enabling proteins to be harvested from transformed leaves within a matter of days.

Using this system, Medicago claims to have produced a virus-like particle of the coronavirus within just 20 daysof the SARS-CoV-2 genetic sequence becoming available. The government of Canada quickly put millions of dollars behind the effort as a result.

Astonishingly, given that the coronavirus pandemic is now threatening to devastate societies and economies around the planet on a scale second only to a world war, this effort is still short of cash. CEPI has issued an urgent call for funding, seeking to raise $2 billion: it says just $375 billion by the end of March would enable four-to-six vaccine candidates to move rapidly towards phase 2/3 trials.

Scientists are also hoping desperately that SARS-CoV-2 does not rapidly mutate as influenza viruses tend to do, which would likely reduce the effectiveness of any single vaccine. So far, according to researchers studying 1,000 samples of the virus from around the world, this seems not to be the case.

This means that the race to find a vaccine, and to do so in sufficient time to salvage the situation before the world tips into an economic depression and millions of people die, has a decent chance of success and that any successful vaccine would likely confer lasting immunity.

Meanwhile, all of humanity is waiting. And if the scientists do succeed in this urgent challenge, it will very likely be due to modern genetics. Though genetic engineering was once a dirty word, it now could literally help save the world.

See the rest here:

Science to the rescue? How modern genetics could help save the world from coronavirus - Alliance for Science - Alliance for Science

The Department of Molecular & Human Genetics has claimed that it has discovered a new technology to test COVID-19 virus and give accurate results within 5-6 hours.

Sangeeta NairMar 31, 2020 14:04 IST

The Department of Molecular & Human Genetics at the Banaras Hindu University has claimed that it has discovered a new technology to test the COVID-19 virus and give accurate results within 5-6 hours.

The departments Associate Professor Dr. Geeta Rai stated that the department had tried to target a protein sequence present only in the COVID-19 virus. We've tried to target a protein sequence present only in COVID19 & not present in any other viral strain, she said.

Dr. Rai added saying, We're hopeful when testing is done it will only detect COVID19 presence, so there'll be less chance of false detection.

The new technology has been developed by an all-women team of BHUs Department of Molecular & Human Genetics. The team includes four researchers- Dr. Geeta Rai, Dolly Das, Khushbupriya and Hiral Thakar.

The research team had filed a patent on March 27, 2020. However, it needs to be validated by the Indian virology research institute- The National Institute of Virology in Pune and after that it would require approval from the Indian Council of Medical Research.

Download our Current Affairs & GK app For exam preparation

See the original post here:

BHU department claims to have discovered new technology to test COVID-19 - Jagran Josh

BOSTON, April 1, 2020 /PRNewswire/ --Stealth Biotherapeutics Corp (NASDAQ: MITO), a clinical-stage biotechnology company focused on the discovery, development and commercialization of novel therapies for diseases involving mitochondrial dysfunction, today reported financial results for the year ended December 31, 2019 and announced recent business highlights.

"We are off to a strong start in 2020, having honed our focus on Barth and our planned expansion into other rare metabolic cardiomyopathies, while continuing to execute on the significant promise of our ophthalmic and other pipeline programs. By decisively reducing expenses in January, our cash and cash equivalents are sufficient through key Barth regulatory interactions in the second half of 2020, bringing us closer to a potential approval with an opportunity for a rare pediatric voucher and expedited regulatory review," said Reenie McCarthy, Chief Executive Officer at Stealth. "We hope to complete enrollment of our Phase 2b study in dry AMD during the second half of this year, keeping us on-track for a second half of 2021 top-line read-out. We are actively planning development initiatives in other rare metabolic cardiomyopathies, on which we hope to engage with the FDA this year. We are also rapidly advancing our pipeline of novel mitochondrial medicines, with SBT-272 being assessed in a Phase 1 clinical trial, preclinical data read-outs expected this year for SBT-272 in amyotrophic lateral sclerosis and multiple system atrophy and SBT-259 in Charcot-Marie-Tooth, and lead optimization underway for our SBT-550 series, targeting the ferroptosis pathway of cell death implicated in neurodegenerative diseases such as Parkinson's."

Fourth Quarter 2019 and Recent Highlights

Key Upcoming Milestones

2019 Financial Results

Revenue: In 2019, the Company recognized $21.1 million in revenue associated with the Alexion arrangement. The revenue represents the portion of the non-refundable upfront payments that were recognized in full upon the delivery of the topline data for the Company's MMPOWER-3 trial. Alexion terminated the arrangement and as such, no additional revenue will be recognized.

Research and Development (R&D) Expenses:R&D expenses decreased by $8.5 million to $44.6 million for the year ended December 31, 2019, from $53.1 million for the year ended December 31, 2018. This decrease was primarily from a net decrease of $8.5 million in clinical trial costs due to the timing of trials that ended in 2018, a $2.8 million decrease in contract manufacturing, and a $0.9 million decrease in discovery related expenses due to timing of activities. These decreases were offset in part by increases of $3.6 million in employee and consultant related expenses driven by continued build-out of clinical, medical affairs and regulatory functions and $0.1 million in other costs.

General and Administrative (G&A) Expenses: G&A expenses increased by $0.1 million to $22.3 million for the year ended December 31, 2019, from $22.2 million for the year ended December 31, 2018. The increase was primarily attributable to a net $2.3 million increase in pre-commercial activities including building market disease awareness, a $1.8 million increase in professional services for activities attributable to operating as a public company, an increase of $3.2 million in employee related costs offset by a decrease of $6.7 million in costs associated with 2018 financing efforts and a decrease in IP legal fees of $0.5 million.

Other Expenses: Other expenses increased by $4.5 million to $25.9 million for the year ended December 31, 2019 from $21.4 million for the year ended December 31, 2018. The increase in other expenses is primarily attributable to a $22.7 million loss on extinguishment of debt recorded with respect to convertible debt conversion into ordinary shares in conjunction with the Company's 2019 initial public offering and a $0.7 million change period over period in the fair value adjustments of the warrant liability. These increases were offset by a $3.4 million change in period over period fair value adjustments of the derivative liability associated with the convertible debt, a decrease in interest expense mostly related to the convertible debt of $14.7 million and an increase in interest income of $0.8 million.

Cash Position: Cash and cash equivalents were $50.8 million at December 31, 2019, compared to $10.9 million at December 31, 2018.

Conference Call

Management will host a conference call today at8:30 am ETto discuss the financial results and provide a general business update. The call can be accessed by dialing (877) 407-0989 or (201) 389-0921 (international) and referencing conference ID 13701108. A live audio webcast of the event can be accessed by visiting the Investors & News section of Stealth's Investor website,https://investor.stealthbt.com/. A replay of the webcast will be archived on Stealth's website for 30 days following the event.

About Stealth

We are a clinical-stage biotechnology company focused on the discovery, development and commercialization of novel therapies for diseases involving mitochondrial dysfunction. Mitochondria, found in nearly every cell in the body, are the body's main source of energy production and are critical for normal organ function. Dysfunctional mitochondria characterize a number of rare genetic diseases and are also involved in many common age-related diseases, typically involving organ systems with high energy demands such as the heart, the eye, and the brain. We believe our lead product candidate, elamipretide, has the potential to treat both rare metabolic cardiomyopathies, such as Barth, Duchenne and Becker muscular dystrophies and Friedreich's ataxia, as well as ophthalmic diseases entailing mitochondrial dysfunction, such as dry age-related macular degeneration and Leber's hereditary optic neuropathy. We are evaluating our second-generation clinical stage candidate, SBT-272, for rare neurodegenerative disease indications following promising preclinical data in amyotrophic lateral sclerosis, or ALS. Our pipeline compounds include SBT-259, which we are evaluating for rare peripheral neuropathies, and the SBT-550 series of compounds, which we plan to evaluate for rare neurodegenerative and ophthalmic indications. We have optimized our discovery platform to identify novel mitochondria-targeted compounds, which may be nominated as therapeutic product candidates or utilized as scaffolds to deliver other compounds to mitochondria. We have assembled a highly experienced management team, board of directors and group of scientific advisors to help us achieve our mission of leading mitochondrial medicine.

Forward-Looking Statements

This press release contains forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995. Such forward-looking statements include those regarding Stealth BioTherapeutics' plans, strategies and expectations for its preclinical and clinical advancement of its drug development programs, including its ongoing clinical trials of elamipretide and planned clinical trial of SBT-272; the potential benefits of Stealth BioTherapeutics' product candidates; its key milestones for 2020; its plans regarding future data presentations; and its financial guidance regarding the period in which it will have capital available to fund its operations. Statements that are not historical facts, including statements about Stealth BioTherapeutics' beliefs, plans and expectations, are forward-looking statements. The words "anticipate," "expect," "hope," "plan," "potential," "possible," "will," "believe," "estimate," "intend," "may," "predict," "project," "would" and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Stealth BioTherapeutics may not actually achieve the plans, intentions or expectations disclosed in these forward-looking statements, and you should not place undue reliance on these forward-looking statements. Actual results or events could differ materially from the plans, intentions and expectations disclosed in the forward-looking statements as a result of known and unknown risks, uncertainties and other important factors, including: Stealth BioTherapeutics' ability to obtain additional funding and to continue as a going concern; the impact of the COVID-19 pandemic; the ability to successfully demonstrate the efficacy and safety of Stealth BioTherapeutics' product candidates and future product candidates; the preclinical and clinical results for Stealth BioTherapeutics' product candidates, which may not support further development and marketing approval; the potential advantages of Stealth BioTherapeutics' product candidates; the content and timing of decisions made by the U.S. FDA, the EMA or other regulatory authorities, investigational review boards at clinical trial sites and publication review bodies, which may affect the initiation, timing and progress of preclinical studies and clinical trials of Stealth BioTherapeutics product candidates; Stealth BioTherapeutics' ability to obtain and maintain requisite regulatory approvals and to enroll patients in its planned clinical trials; unplanned cash requirements and expenditures; competitive factors; Stealth BioTherapeutics' ability to obtain, maintain and enforce patent and other intellectual property protection for any product candidates it is developing; and general economic and market conditions. These and other risks are described in greater detail under the caption "Risk Factors" included in the Stealth BioTherapeutics' most recent Annual Report on Form 20-F filed with the Securities and Exchange Commission ("SEC"), as well as in any future filings with the SEC. Forward-looking statements represent management's current expectations and are inherently uncertain. Except as required by law, Stealth BioTherapeutics does not undertake any obligation to update forward-looking statements made by us to reflect subsequent events or circumstances.

Investor RelationsStern Investor RelationsLauren Stival, 212-362-1200IR@StealthBT.com

STEALTH BIOTHERAPEUTICS CORP

Condensed Consolidated Balance Sheets

(inthousands)

December 31,

December 31,

2019

2018

Assets

Current assets:

Cash and cash equivalents

$ 50,768

$ 10,855

Prepaid expenses and other current assets

1,630

2,438

Total current assets

52,398

13,293

Property and equipment, net

345

499

Deferred offering costs

1,325

Other non-current assets

406

Total assets

$ 52,743

$ 15,523

Liabilities, convertible preferred shares andshareholders' equity (deficit)

Current liabilities:

Accounts payable

$ 9,520

$ 11,023

Accrued expenses and other current liabilities

8,495

13,826

Accrued interest payable

1,219

7,297

Current portion of long-term debt

14,716

8,465

Total current liabilities

33,950

40,611

Long-term debt, less current portion

1,526

10,317

Convertible notes payable

103,257

Derivative liability

36,567

Warrant liability

100

Total liabilities

35,476

190,852

Series A convertible preferred shares

211,377

Total shareholders' equity (deficit)

17,267

(386,706)

Total liabilities, convertible preferred shares andshareholders' equity (deficit)

$ 52,743

$ 15,523

STEALTH BIOTHERAPEUTICS CORP

Condensed Consolidated Statements of Operations

(inthousands,exceptshareandpersharedata)

Year Ended December 31,

2019

2018

Revenue

View post:

Stealth BioTherapeutics Reports Fiscal Year 2019 Financial Results And Recent Business Highlights - BioSpace

Universityof Toronto researcherSachdev Sidhuand his collaborators are engineering antibody molecules that can neutralize the novel coronavirus in the body before it invades cells.

Sidhu (left) already leads a differentteam that received supportin the first round of federal funding. The goal of that project is to design antiviral medicines that block viral replication.

With our two funded projects, we are working to develop molecules that can target the virus both inside human cells and on the outside to prevent it from getting in, says Sidhu, who is a professor of molecular genetics in the Faculty of Medicine.

Other teams in Canada, as well as in the U.K. and U.S., are looking to infuse Covid-19 survivors blood plasma containing antibodies into patientsto aid their recovery. Plasma transfusion, however, is fraught with challenges, including variability in efficacy between different donors and risk of disease transmission. Synthetic antibodies, on the other hand, represent a defined drug in terms of molecular content, efficacy and dosing regimen.

Rini has previously helped to determine how antibodies bind to and inactivate the SARS virus, the coronavirus that caused the outbreak in Asia more than 15 years ago. Also on the team isAlan Cochrane, a professor in the department of molecular genetics and an HIV virologist with expertise in viral RNA processing.

The antibodies will be engineered to block the so-called S-protein that forms spikes on the virus's surface. The spikes lock on to a protein called ACE2 on the surface of human cells to gain entry. Coating viral particles with synthetic antibodies should prevent the spikes from binding to ACE2.

Sidhu and Rini will also engineer antibodies that bind ACE2 to make it inaccessible to the virus. This type of engineered immunity surpasses the capacity of the bodys natural immune system since antibodies that react against self-proteins have been filtered out. If successful, the approach may obviate worries about viral mutations that can render drugs ineffective to new emerging viral strains becausethe host protein ACE2 does not change over time.

Sidhus team has advanced a technology called phage display to rapidly create and select human antibodies with desired biological properties, including blocking the virussspike protein. Over the last decade, his team has created hundreds of antibodies with therapeutic potential some of which are in clinical development through spin-off companiesand large pharmaceutical firms.

The group has demonstrated success with both approaches for inhibiting viral entry, having developed neutralizing antibodies that target the Ebola virus as well as antibodies that target the human host receptor of hantavirus or hepatitis C. Moreover, other research has shown that antibodies targeting SARS, a related virus whose genetic material is over 80 per cent identical to the one causing COVID-19, can clear infection in cells and mice.

Using phage display, in which tiny bacterial viruses called phages are instructed to create vast libraries of diverse antibodies, the team will select the antibodies that can kill the virus in human cells before testing them on mice and, eventually, patients. Experiments on mice could start within three to six months, Sidhu says.

In addition to creating antibodies tailored to the new virus from scratch, the researchers will also modify existing SARS-blocking antibodies so that they attack COVID-19 and provide an additional route to the development of a therapeutic.

Given the global spread of the virus, its possible that it will become endemic and circulate in the population like seasonal flu. And, like the flu, it could mutate into new strains that will evade acquired immunity and the vaccines that are being developed. By generating a panel of different antibodies, the researchers aim to stay one step ahead of the virus.

Our advances in antibody engineering technologiesand access to the complete genomes of the COVID-19 virus and its relatives provides us with an opportunity to create tailored therapeutic antibodies at a scale and speed that was not possible even a few years ago, says Sidhu.

Ultimately, we aim to optimize methods to the point where the evolution of new drugs will keep pace with the evolution of the virus itself, providing new and effective drugs in response to new outbreaks.

Originally posted here:

Researchers at U of T developing antibodies to 'neutralize' novel coronavirus before it invades cells - News@UofT

Coronavirus. Just the word strikes fear into our hearts.

Novel coronavirus is the proper term for this brand-new virus wreaking havoc on our unprepared world.

But you can also call this nasty villain by its scientific name: severe acute respiratory syndrome coronavirus 2, or SARS-CoV-2 for short.

Becoming infected with SARS-CoV-2 can trigger a potentially deadly respiratory disease called Covid-19, an illness which presents with three main acute symptoms: fever, a deep, dry cough and a shortness of breath which can become quickly life-threatening. Other symptoms can mimic a cold or the flu.

Covid-19 seems to strike the elderly and immunocompromised the hardest, along with any of us with underlying health conditions such as diabetes, heart and lung disease. But the young shouldnt take anything for granted there have been numerous deaths among people aged 20 to 50, as well as a very few among children.

Covid-19 can also present with mild symptoms very similar to a typical cold or flu or no symptoms at all, which makes controlling the spread of the virus causing Covid-19 very difficult.

All viruses are like zombies they try to take over peoples bodies but they arent really alive. Outside the hosts body they are dormant, surviving without living. Once touched or inhaled and brought inside, their ancient machinery springs into action, using proteins to latch onto and invade human cells.

There they set up shop, producing millions of copies of themselves and causing those cells to rupture. Like the famous scene from the movie Alien, the viral offspring shoot out into the bloodstream, with the goal of invading more and more cells.

As they multiply, humans began to spit them out into the universe with each exhalation, making us contagious days before we begin to cough, sneeze or have diarrhea all symptoms the virus creates to ensure it can leap from human to human, thus ensuring its survival.

This virus zombie invasion comes in all sort of shapes, sizes and genetic strategies. All coronaviruses are covered with pointy spires of protein, giving them the appearance of having a crown or corona hence the name. Coronaviruses use these spikes to latch onto and pierce our cells.

Coronaviruses are part of the RNA brigade of viruses, which are much less stable than their DNA-based comrades. Why is that important? Because instability leads to mistakes in copying genetic code.

That leads to mutations thousands, millions, billions of mutations. Sooner or later, one mutation hits pay dirt and allows the virus to cross the great divide between different species. A few million/billion/trillion more mistakes creates another mutation that allows that virus to spread easily. Now the virus is both in its new host and it is contagious.

Its that type of mutation which gives humanity viruses like SARS-CoV-2.

The animal kingdom is teeming with coronaviruses. They are found in cats and dogs, pigs and cattle, turkey and chickens, mice, rats, rabbits and of course, humans. Insects too.

Some of those coronviruses can cross species, such as between pigs, cats and dogs, but for the most part coronaviruses stay loyal to their original hosts. Until, of course, they become that lucky mutation.

Usually viruses from one animal really dont effectively transmit to other animal species or even to people, said Dr. John Williams, chief of the division of pediatric infectious diseases at the University of Pittsburgh Medical Center Childrens Hospital of Pittsburgh.

So usually if a virus goes from an animal to a human, its sort of dead end. That person gets sick but it doesnt spread further, said Williams, who has studied coronaviruses for decades.

Besides the newly hatched novel coronavirus, there are actually six additional coronaviruses that infect humans four of them cause the common cold.

Two more can be deadly. MERS-CoV is the villian behind Middle East Respiratory Syndrome, or MERS, which has killed over 800 people worldwide since it first appeared in 2012.

SARS-CoV causes a serious form of pneumonia that can also be life-threatening. Globally, it killed 774 people between 2002 and 2004. No other cases have been reported worldwide since. {To put that into context, the death toll of the novel coronavirus since it burst on the scene in December is approaching 40,000).

The coronaviruses that cause MERS and SARS are though to have crossed from mammals to humans, where they mutated to become contagious. MERS-CoV first appeared in Jordon and Saudi Arabia in 2012 and its thought to have crossed over to humans from dromedary camels in Africa, the Middle East and southern Asia.

MERS is extremely deadly, about 30% of people who are infected with MERS will die, Williams said. So the virus got over one of the barriers its able to infect humans, grow in them and cause disease but thankfully it really doesnt spread well person to person, other than very, very close contacts.

SARS has been more difficult to pin down.

Because one of the most common carriers for coronaviruses are bats, its thought that the virus may have started there. Then it supposedly mutated to the masked palm civet, a small cat-like mammal eaten in some parts of China. But even that theory is disputed.

SARS caused death in about 10% of people that became infected and it did spread person to person but not super effectively, Williams said. There werent many people walking around without symptoms or with mild symptoms, who could be spreading it.

This new virus, SARS-CoV-2, has overcome more barriers, Williams added. It spreads easily person to person and a lot of people can have either mild disease or they might not even have symptoms, yet they can have the virus and spread it.

The novel coronavirus appears to have originated in bats. A study published in February found the coronavirus found in bats shared 96% of the same genetic makeup as the novel coronavirus. But it wasnt a direct link, so the bat had to have infected another species, which then infected humans.

Early reports pointed to snakes bought at a wet market in China were people buy live animals to eat. A recent report of the initial cases of coronavirus in China debunks the snake flu theory, reporting that in 13 of the 41 early cases the infected patients had no link to the wet market.

A recent hypothesis claimed the intermediate host was the pangolin, an endangered scaly, ant-eating creature beloved for its meat and scales, which are used in traditional Chinese medicine. But critics have been skeptical, sending genetic scientists back to their labs to continue the search.

At this time, scientists dont know where the novel coronavirus began.

These things are more difficult than [identifying] dinosaurs, because theres no fossil record of a virus, Williams said. For example, the main virus I study, human metapneumovirus, is clearly a virus that has circulated in humans for decades if not a few centuries.

However, when you look at the genetics of the virus, its closest genetic relative is a bird virus, he added. So, did that virus jump to humans way back and become established? Thats what we think. But it isnt impossible that a human virus jumped to birds and became established there.

See the original post here:

What is coronavirus and Covid-19? An explainer - KTVZ

An erudite report of a worldwide Plasmid Market is recently published by Absolute Markets Insights. The statistical report offers an appropriate analysis of recent trends and technological advancements in global regions such as North America, Latin America, Asia-Pacific, Africa, and India. The data further also applies useful tools, methodologies and standard operating procedures carried out by top-level industries to support its analysis. Moreover, it also applies other effective exploratory techniques such as primary and secondary research techniques.

A plasmid is a small, circular piece of deoxyribonucleic acid (DNA), which is all the genetic material found in an organisms chromosomes and replicates independently of chromosomal DNA. Worldwide rising awareness levels about gene therapy across the globe in recent years is fostering the market growth. According to an article published by Human Gene Therapy, the adoption of gene therapy for chronic diseases, which include Alzheimer Disease is high around the world as compared to less severe diseases, namely, attention deficit hyperactivity disorder (ADHD). Gene therapy is a promising treatment option for various diseases such as inherited disorders, some types of cancer, and certain viral infections; and most commonly, gene therapy is an approach to treat the genetic disorders. Rising number of clinical trials related to gene therapy coupled with increasing funding for research and development activities is likely to nourish the global plasmid market during the forecast period. Surging waves of advanced genetic information have marked the advent of gene therapy revolution in the recent decade. The profound knowledge about gene therapy has accelerated the potential of human genetics and disease, therefore paving the way for gene therapy in pharmaceuticals in the 21st century.

Request a Sample@ https://www.absolutemarketsinsights.com/request_sample.php?id=363

Major participants in the global plasmid market are adopting growth strategies such as new product launches, mergers and acquisitions, collaborations, partnerships, geographical and operational expansions, among others in order to gain a competitive advantage. For instance, in July 2019, Mirus Bio LLC launched TransIT-VirusGEN SELECT Transfection Reagent, which was designed for the drug discovery pipeline in gene and cell therapy manufacturing process.

Some of the distinctive market key components of the global Plasmid Market have been studied in order to get accurate market information about the requirements of the businesses. Financial and economic aspects of the businesses are also presented by means of graphical presentation techniques such as charts, graphs, tables, and pictures. The entire demand and supply chain is explained with the help of penetrative insight into the businesses.

Enquiry Before Buying@ https://www.absolutemarketsinsights.com/enquiry_before_buying.php?id=363

Key Findings of the Report:

Request for Customization@ https://www.absolutemarketsinsights.com/request_for_customization.php?id=363

Global Plasmid Market:

By General Type Plasmid

By Specific Plasmid Types

By Application

By Region

Get Full Information of this premium report@ https://www.absolutemarketsinsights.com/reports/Plasmid-Market-2019-2027-363

About Us:

Absolute Markets Insights assists in providing accurate and latest trends related to consumer demand, consumer behavior, sales, and growth opportunities, for the better understanding of the market, thus helping in product designing, featuring, and demanding forecasts. Our experts provide you the end-products that can provide transparency, actionable data, cross-channel deployment program, performance, accurate testing capabilities and the ability to promote ongoing optimization.

From the in-depth analysis and segregation, we serve our clients to fulfill their immediate as well as ongoing research requirements. Minute analysis impact large decisions and thereby the source of business intelligence (BI) plays an important role, which keeps us upgraded with current and upcoming market scenarios.

Contact Us:

Company: Absolute Markets Insights

Email id: sales@absolutemarketsinsights.com

Phone: +91-740-024-2424

Contact Name: Shreyas Tanna

The Work Lab,

Model Colony, Shivajinagar, Pune, MH, 411016

Website: https://www.absolutemarketsinsights.com/

Originally posted here:

Plasmid Market was Valued at US$ 89.52 million in 2018 and is Estimated to Reach US$ 447.68 Million by 2027, growing at a CAGR of 19.5% over the...

The genetic architecture of the human cerebral cortex

By Katrina L. Grasby, Neda Jahanshad, Jodie N. Painter, Luca Colodro-Conde, Janita Bralten, Derrek P. Hibar, Penelope A. Lind, Fabrizio Pizzagalli, Christopher R. K. Ching, Mary Agnes B. McMahon, Natalia Shatokhina, Leo C. P. Zsembik, Sophia I. Thomopoulos, Alyssa H. Zhu, Lachlan T. Strike, Ingrid Agartz, Saud Alhusaini, Marcio A. A. Almeida, Dag Alns, Inge K. Amlien, Micael Andersson, Tyler Ard, Nicola J. Armstrong, Allison Ashley-Koch, Joshua R. Atkins, Manon Bernard, Rachel M. Brouwer, Elizabeth E. L. Buimer, Robin Blow, Christian Brger, Dara M. Cannon, Mallar Chakravarty, Qiang Chen, Joshua W. Cheung, Baptiste Couvy-Duchesne, Anders M. Dale, Shareefa Dalvie, Tnia K. de Araujo, Greig I. de Zubicaray, Sonja M. C. de Zwarte, Anouk den Braber, Nhat Trung Doan, Katharina Dohm, Stefan Ehrlich, Hannah-Ruth Engelbrecht, Susanne Erk, Chun Chieh Fan, Iryna O. Fedko, Sonya F. Foley, Judith M. Ford, Masaki Fukunaga, Melanie E. Garrett, Tian Ge, Sudheer Giddaluru, Aaron L. Goldman, Melissa J. Green, Nynke A. Groenewold, Dominik Grotegerd, Tiril P. Gurholt, Boris A. Gutman, Narelle K. Hansell, Mathew A. Harris, Marc B. Harrison, Courtney C. Haswell, Michael Hauser, Stefan Herms, Dirk J. Heslenfeld, New Fei Ho, David Hoehn, Per Hoffmann, Laurena Holleran, Martine Hoogman, Jouke-Jan Hottenga, Masashi Ikeda, Deborah Janowitz, Iris E. Jansen, Tianye Jia, Christiane Jockwitz, Ryota Kanai, Sherif Karama, Dalia Kasperaviciute, Tobias Kaufmann, Sinead Kelly, Masataka Kikuchi, Marieke Klein, Michael Knapp, Annchen R. Knodt, Bernd Krmer, Max Lam, Thomas M. Lancaster, Phil H. Lee, Tristram A. Lett, Lindsay B. Lewis, Iscia Lopes-Cendes, Michelle Luciano, Fabio Macciardi, Andre F. Marquand, Samuel R. Mathias, Tracy R. Melzer, Yuri Milaneschi, Nazanin Mirza-Schreiber, Jose C. V. Moreira, Thomas W. Mhleisen, Bertram Mller-Myhsok, Pablo Najt, Soichiro Nakahara, Kwangsik Nho, Loes M. Olde Loohuis, Dimitri Papadopoulos Orfanos, John F. Pearson, Toni L. Pitcher, Benno Ptz, Yann Quid, Anjanibhargavi Ragothaman, Faisal M. Rashid, William R. Reay, Ronny Redlich, Cline S. Reinbold, Jonathan Repple, Genevive Richard, Brandalyn C. Riedel, Shannon L. Risacher, Cristiane S. Rocha, Nina Roth Mota, Lauren Salminen, Arvin Saremi, Andrew J. Saykin, Fenja Schlag, Lianne Schmaal, Peter R. Schofield, Rodrigo Secolin, Chin Yang Shapland, Li Shen, Jean Shin, Elena Shumskaya, Ida E. Snderby, Emma Sprooten, Katherine E. Tansey, Alexander Teumer, Anbupalam Thalamuthu, Diana Tordesillas-Gutirrez, Jessica A. Turner, Anne Uhlmann, Costanza Ludovica Vallerga, Dennis van der Meer, Marjolein M. J. van Donkelaar, Liza van Eijk, Theo G. M. van Erp, Neeltje E. M. van Haren, Daan van Rooij, Marie-Jos van Tol, Jan H. Veldink, Ellen Verhoef, Esther Walton, Mingyuan Wang, Yunpeng Wang, Joanna M. Wardlaw, Wei Wen, Lars T. Westlye, Christopher D. Whelan, Stephanie H. Witt, Katharina Wittfeld, Christiane Wolf, Thomas Wolfers, Jing Qin Wu, Clarissa L. Yasuda, Dario Zaremba, Zuo Zhang, Marcel P. Zwiers, Eric Artiges, Amelia A. Assareh, Rosa Ayesa-Arriola, Aysenil Belger, Christine L. Brandt, Gregory G. Brown, Sven Cichon, Joanne E. Curran, Gareth E. Davies, Franziska Degenhardt, Michelle F. Dennis, Bruno Dietsche, Srdjan Djurovic, Colin P. Doherty, Ryan Espiritu, Daniel Garijo, Yolanda Gil, Penny A. Gowland, Robert C. Green, Alexander N. Husler, Walter Heindel, Beng-Choon Ho, Wolfgang U. Hoffmann, Florian Holsboer, Georg Homuth, Norbert Hosten, Clifford R. Jack Jr., MiHyun Jang, Andreas Jansen, Nathan A. Kimbrel, Knut Kolskr, Sanne Koops, Axel Krug, Kelvin O. Lim, Jurjen J. Luykx, Daniel H. Mathalon, Karen A. Mather, Venkata S. Mattay, Sarah Matthews, Jaqueline Mayoral Van Son, Sarah C. McEwen, Ingrid Melle, Derek W. Morris, Bryon A. Mueller, Matthias Nauck, Jan E. Nordvik, Markus M. Nthen, Daniel S. OLeary, Nils Opel, Marie-Laure Paillre Martinot, G. Bruce Pike, Adrian Preda, Erin B. Quinlan, Paul E. Rasser, Varun Ratnakar, Simone Reppermund, Vidar M. Steen, Paul A. Tooney, Fbio R. Torres, Dick J. Veltman, James T. Voyvodic, Robert Whelan, Tonya White, Hidenaga Yamamori, Hieab H. H. Adams, Joshua C. Bis, Stephanie Debette, Charles Decarli, Myriam Fornage, Vilmundur Gudnason, Edith Hofer, M. Arfan Ikram, Lenore Launer, W. T. Longstreth, Oscar L. Lopez, Bernard Mazoyer, Thomas H. Mosley, Gennady V. Roshchupkin, Claudia L. Satizabal, Reinhold Schmidt, Sudha Seshadri, Qiong Yang, Alzheimers Disease Neuroimaging Initiative, CHARGE Consortium, EPIGEN Consortium, IMAGEN Consortium, SYS Consortium, Parkinsons Progression Markers Initiative, Marina K. M. Alvim, David Ames, Tim J. Anderson, Ole A. Andreassen, Alejandro Arias-Vasquez, Mark E. Bastin, Bernhard T. Baune, Jean C. Beckham, John Blangero, Dorret I. Boomsma, Henry Brodaty, Han G. Brunner, Randy L. Buckner, Jan K. Buitelaar, Juan R. Bustillo, Wiepke Cahn, Murray J. Cairns, Vince Calhoun, Vaughan J. Carr, Xavier Caseras, Svenja Caspers, Gianpiero L. Cavalleri, Fernando Cendes, Aiden Corvin, Benedicto Crespo-Facorro, John C. Dalrymple-Alford, Udo Dannlowski, Eco J. C. de Geus, Ian J. Deary, Norman Delanty, Chantal Depondt, Sylvane Desrivires, Gary Donohoe, Thomas Espeseth, Guilln Fernndez, Simon E. Fisher, Herta Flor, Andreas J. Forstner, Clyde Francks, Barbara Franke, David C. Glahn, Randy L. Gollub, Hans J. Grabe, Oliver Gruber, Asta K. Hberg, Ahmad R. Hariri, Catharina A. Hartman, Ryota Hashimoto, Andreas Heinz, Frans A. Henskens, Manon H. J. Hillegers, Pieter J. Hoekstra, Avram J. Holmes, L. Elliot Hong, William D. Hopkins, Hilleke E. Hulshoff Pol, Terry L. Jernigan, Erik G. Jnsson, Ren S. Kahn, Martin A. Kennedy, Tilo T. J. Kircher, Peter Kochunov, John B. J. Kwok, Stephanie Le Hellard, Carmel M. Loughland, Nicholas G. Martin, Jean-Luc Martinot, Colm McDonald, Katie L. McMahon, Andreas Meyer-Lindenberg, Patricia T. Michie, Rajendra A. Morey, Bryan Mowry, Lars Nyberg, Jaap Oosterlaan, Roel A. Ophoff, Christos Pantelis, Tomas Paus, Zdenka Pausova, Brenda W. J. H. Penninx, Tinca J. C. Polderman, Danielle Posthuma, Marcella Rietschel, Joshua L. Roffman, Laura M. Rowland, Perminder S. Sachdev, Philipp G. Smann, Ulrich Schall, Gunter Schumann, Rodney J. Scott, Kang Sim, Sanjay M. Sisodiya, Jordan W. Smoller, Iris E. Sommer, Beate St Pourcain, Dan J. Stein, Arthur W. Toga, Julian N. Trollor, Nic J. A. Van der Wee, Dennis van t Ent, Henry Vlzke, Henrik Walter, Bernd Weber, Daniel R. Weinberger, Margaret J. Wright, Juan Zhou, Jason L. Stein, Paul M. Thompson, Sarah E. Medland, Enhancing NeuroImaging Genetics through Meta-Analysis Consortium (ENIGMA)Genetics working group

Science20 Mar 2020

Read the original here:

The genetic architecture of the human cerebral cortex - Science Magazine

NEW YORK, March 25, 2020 /PRNewswire/ -- Kallyope Inc., a leading biotechnology company focused on identifying and pursuing therapeutic opportunities involving the gut-brain axis, today announced a $112 million Series C financing. This financing will be used to advance its portfolio of programs and the company's first clinical trials, further establishing its leadership in the gut-brain axis field.

All investors from the Series B financing participated in the Series C round, including The Column Group, Lux Capital, Polaris Partners, Euclidean Capital, Two Sigma Ventures, Illumina Ventures, Alexandria Venture Investments, and Bill Gates. New investors include Casdin Capital, Greenspring Associates, and two unnamed leading institutional investors.

"Four years ago, we started our journey to build a preeminent biotech based in New York City as a first-mover in the gut-brain axis space. Now, this Series C financing will enable us to advance multiple programs to clinical development," said Kallyope CEO Nancy Thornberry.

The Series C financing comes after four highly productive years in which Kallyope has built a portfolio of programs directed to novel targets in a wide array of diseases. In support of these programs, the company has established industry-leading capabilities in designing oral small-molecule drugs that selectively target the gut but not the rest of the body.

The company today also announced its lead program targeting satiety circuits for weight loss, with clinical testing expected to begin later this year. A second program targeting gut barrier function with potential relevance for inflammatory bowel disease (IBD) and several other diseases is anticipated to enter the clinic soon after. In addition, the company continues to advance a broad portfolio of programs for gastrointestinal, CNS, and inflammatory disorders.

"Kallyope pursues programs where the company's platform provides an edge over other approaches and where we have an opportunity to deliver major clinical benefits rather than incremental improvements over current treatments. We are targeting neural and hormonal circuits, including novel vagal circuits, involved in a broad array of physiology and disease," said Thornberry.

"Kallyope has made significant progress since the company's inception in late 2015. Its platform is enabling a mechanistic understanding of the gut-brain axis, which in turn has revealed new, actionable biology that the company is now exploring in several promising programs. I believe that Kallyope's platform and rigorous approach to identifying, characterizing, and targeting gut-brain circuits with gut-restricted small molecules has greatly increased its odds of success in clinical studies," said Kallyope co-founder and board member Tom Maniatis, Ph.D.

About Kallyope Inc.

Kallyope, headquartered at the Alexandria Centerfor Life Science in New York City, is a biotechnology company dedicated to unlocking the therapeutic potential of the gut-brain axis. The company's cross-disciplinary team integrates advanced technologies in sequencing, bioinformatics, neural imaging, cellular and molecular biology, and human genetics to provide an understanding of gut-brain biology that leads to transformational therapeutics to improve human health. The company's founders are Charles Zuker, Ph.D., Lasker Award winner Tom Maniatis, Ph.D., and Nobel laureate Richard Axel, M.D. For more information visitwww.kallyope.com.

Contact

Morgan Warners (202) 337-0808mwarners@gpg.com

View original content to download multimedia:http://www.prnewswire.com/news-releases/kallyope-inc-announces-112m-series-c-financing-to-support-first-clinical-trials-and-advance-portfolio-of-programs-targeting-the-gut-brain-axis-301029250.html

SOURCE Kallyope Inc.

Original post:

Kallyope Inc. Announces $112M Series C Financing to Support First Clinical Trials and Advance Portfolio of Programs Targeting the Gut-Brain Axis - P&T...

The common fruit fly which lives one to two months, suggesting insignificance has changed the world through medical research, leading to eight Nobel prizes in human genetics and disease prevention breakthroughs. Today an even smaller organism, Coronavirus, is changing the world even more significantly.

And confronting it with the same opportunity for breakthroughs as scientists treated fruit flies could hold the key to solving our greatest challenge climate change.

Of course, all of the coronaviruses impacts sickness, deaths, economic crises have been negative. But, like the scientists who saw something unique in the fruit fly instead of just an unwelcome pest, coronavirus offers us a unique opportunity: visceral lessons in how to approach future crises, and the horrible costs of not doing so.

First among those lessons is taking authoritative warnings seriously, even when that may result in tough decisions. We have been warned repeatedly over the last decade that a pandemic was an existential threat to our way of life. At the end of 2019, when the late Chinese doctor Li Wenliang first reported his alarm over a coronavirus outbreak, authorities detained him for spreading rumors. If they had acted on his warning, the spread in China would have been less severe.

But by January 21, 2020 China had 278 confirmed cases, other countries had 282, and the World Health Organization issued its first coronavirus advisory. Instead of preparing for the virus inevitable spread to the United States, President Donald Trump downplayed the risk, comparing it to a bad case of the flu. Two months later, tens of thousands of Americans have tested positive for the virus and millions more are under shelter-in-place rules, threatening to send the global economy into a devastating tailspin.

Unfortunately, weve consistently made these same mistakes of ignoring scientific warnings when dealing with other global crises, especially climate change. Beginning in June 1988, when climate scientist James Hansen warned Congress that global warming had begun, climate scientists predictions have repeatedly and increasingly warned of impending crises, and how climate change is accelerating faster than expected much like the Coronavirus. Sadly, the government response has ranged from non-existent to lacking.

Thirty years after Hansens warning, President Trump dismissed an official U.S. government assessment of climate changes risks in 2018, saying I dont believe it. As temperatures have risen, so too has the cost of inaction. From 1979 to 2017, the cost of global climate change-related disasters has increased 150%, costing $2.25 trillion, with the U.S. bearing the brunt of the financial pain at $945 billion nearly twice Chinas second-highest total of $492 billion.

Fortunately, in the battle against coronavirus, countries like South Korea that embrace science-based health warnings and act decisively are able to flatten the curve of the coronavirus spread to reduce infections and deaths. But when it comes to climate change, despite global accords such as the Paris Agreement, the world is still struggling to act decisively and in unison.

The Trump administration stands out with its rejection of science-based climate change policy, compounding decades of foot dragging by rolling back and undermining Obama administration efforts to rein in and reduce greenhouse gas emissions from coal, oil, and auto tailpipes. As of the end of 2019, a New York Times analysis identified 95 environmental rules that are being rolled back by the White House.

A key Trump environmental program roll back is expected to be finalized by the end of March. The administration is relaxing the auto greenhouse gas and fuel economy standards that President Obama announced in 2012. The first national program to reduce transportation greenhouse gas emissions, it was based on science, engineering capabilities, business capacities, as well as environmental and health benefits. It would have doubled fuel economy to 54.5 miles per gallon (mpg) by 2025, eliminated 6 billion tons of carbon dioxide, and saved consumers $1.7 trillion at the pump. It appeared the U.S. was finally listening to climate scientists.

But in early 2017 with Trump at the helm, the auto industry, amidst several years of record sales and profits, found an opportunity to renege on its commitment to the standards and asked the White House to relax the Obama administrations standards. After extensive analysis, the U.S. Environmental Protection Agencys scientists and auto engineers had recently re-affirmed the program. But facts were no longer in control of the process.

The final rule targets the standards for the 2021-2026 period. It is widely expected to pull back the standards to 37 mpg and reduce the annual fuel economy improvement to 1.5%, down from the current 5%.

Here is the rub. Transportation is now the fastest growing sector driving increased U.S. greenhouse gas emissions. Even the Obama administrations standards, which the Trump administration is trying to scale back, were never enough to address this gorilla in the room. A landmark study by the National Academy of Science in 2013 calculated that the worlds entire fleet of vehicles in 2025 would have to average around 180 mpg to limit warming to safe levels. As detailed in my book, Driving the Future, if we achieved the original 2025 target and enacted rules to continue the 5% annual improvement curve through 2050, we would only reach 80% of the target required to meet the Intergovernmental Panel on Climate Changes (IPCC) earlier target of 2C target of safe warming and the gap will be even greater to reach the new IPCC target of 1.5C.

The only pathway to reaching the IPCCs targets is transportation electrification. The administration should abandon the new rules they are developing, leave the current rules in place and begin work on the post 2025 standards. The auto industry has four to five year planning horizons and needs policy certainty. The world needs to avoid the scale of disruptions that climate change will bring even if the slow pace is deceiving.

The current coronavirus crisis has produced one near-miracle: The bitterly partisan U.S. Congress and federal government are quickly negotiating emergency legislation to deal with the public health and economic crises. Hopefully, reliance on science-based health measures will now guide the countrys approach to combatting coronavirus. And, while the world awaits the worst yet to come in coronavirus infections and deaths, the lessons from this pandemic could result in an approach to bi-partisan, scientifically driven commitment to combat climate change.

Like the seemingly insignificant fruit fly, confronting greenhouse gas and fuel economy standards could produce outsized breakthroughs on climate change. Like the coronavirus, listening to scientific warnings about climate change before it is too late could prevent outsized public health and economic tragedies.

And no, this is not a dream. The reality of global disruption is staring us all in the face. Blinking is not an option.

See the original post here:

The Coronavirus Pandemic Shows Us The Importance Of Combatting Climate Change - Forbes

Veralox Therapeutics is a startup currently headquartered at the Frederick Innovation Technology Center, Inc. (FITCI) in Frederick, Maryland. As a small molecule therapeutics company focused on developing medicines targeting the arachidonic acid pathway, they have two drug products in development for the treatment of a rare blood disorder known as heparin-induced thrombocytopenia and thrombosis and Type 1 Diabetes.

The BioBuzz team recently caught up with Veraloxs CEO Dr. Jeff Strovel, who spoke about the genesis of Veralox, its advancing pipeline, the companys recent milestones and its outlook for the future.

Tell our audience a bit about the founding of Veralox Therapeutics

Ill never forget the day a trusted colleague, David Maloney, called me when I was driving back to my office. He told me he had been working to develop a clinical candidate that selectively targeted the arachidonic acid (AA) pathway through inhibition of a protein called 12-Lipoxygenase. He believed the program was ready to be brought into a company, and there was potential for broad therapeutic utility of the inhibitor, which was intriguing. I have heard a lot of drug program pitches and usually get a sense of where the holes are pretty quickly. In this case, we talked for 30 minutes and afterward I knew this program was ready for company formation. Our first product in development, VLX-1005, is for treatment of the rare blood disorder heparin-induced thrombocytopenia & thrombosis (HITT) which also happens to be the same blood disorder that nearly killed my father years ago. We started the company in 2017 along with Daves colleague from the NCATS (National Center for Advancing Translational Sciences) at the NIH, Matt Boxer, with our rare disease blood disorder drug as our lead candidate. I feel the stars really aligned for us and we have been charging ahead ever since.

Dave, in collaboration with several other partners, led the development of our lead candidate, VLX-1005 while he was a chemistry Group Leader at NCATS.

What is your life science background and what did you do prior to co-founding Veralox?

I hold a Ph.D. in Human Genetics from the University of Maryland School of Medicine. I then went on to be a clinical cytogenetics fellow at the National Cancer Institute Department of Pathology at the NIH. While at NIH I developed a drug target ID platform that got the interest of companies doing cancer drug discovery and I eventually joined a company called Avalon, where I worked in drug discovery and development for about 9 years and served my last two years as Head of Translational Oncology. I learned a great deal about the drug discovery and development process during my time there.

After Avalon I was part of a group of local life science veterans that co-founded the Clinical Research Organization (CRO) Noble Life Sciences. The CRO also served as a kind of incubator for new companies. We incubated several new companies like Neximmune and Convergene Pharmaceuticals, where I served as Chief Scientific Officer and President from 2011 to 2015 before taking on the Chief Executive role from 2015 to 2017. During that time I had met and worked with Dave and I left Convergene to start Veralox with him and our other co-founder Matthew Boxer.

What is Veraloxs lead drug candidate, what disease does it target and where does it sit in the development process?

Our lead drug candidate is for the treatment of patients with HITT, which is a rare, life-threatening disease caused by an immune reaction to Heparin. This drug candidate is a small molecule product that inhibits the 12-lipoxygenase (12-LOX) enzyme which produces 12-HETE. Both 12-LOX and 12-HETE are implicated in numerous diseases. The only FDA-approved drug for HIT/HITT, argatroban, doesnt treat the underlying cause of the disease and has significant potential side effects leaving a significant unmet need.

There are approximately 50,000 people that will be diagnosed with HIT/HITT in the US this year but the number of those treated for this disease is approximately 150,000 annually. HIT takes time to diagnose and doctors cant wait for a definitive diagnosis to make treatment decisions. If patients are suspected of having the disease they must be treated immediately given the risk for deadly thrombosis. The current approved treatment, argatroban, can cause major bleeds which in and of itself can lead to death in these patients. Better drugs are needed that address the pathology of the disease without contributing potentially lethal side effects.

Our HIT treatment inhibits the underlying pathophysiology of HITT to halt the aberrant immune response driving the disease and essentially offering the potential of a curative modality.

Weve been strategically focused on HIT/HITT, but our approach has potential for a number of other indications. For our HIT/HITT drug candidate, weve submitted our Orphan Drug application and our pre-IND (Investigational New Drug) briefing book to the FDA; we expect to have our GMP material soon and to start GLP toxicology studies in the second quarter of this year. Our team expects to submit the IND for our lead candidate by the end of 2020. We are also co-developing a small molecule, orally administered drug product. We plan to advance this candidate for the treatment for Type 1 Diabetes, which is about a year behind our HIT/HITT clinical candidate.

What are some recent Veralox funding milestones and what are the companys next funding steps?

Weve had success raising capital from grants and venture capital groups. Veralox received about 300K from NIHs Small Business Innovation Research (SBIR) Fund, Phase I, and $300K from NIHs Small Business Technology Transfer (STTR) Fund. We also recently closed a $5.4M seed round that was co-led by Sanofi Ventures and the JDRF T1D Fund and included participation from the VTC Innovation and VTC Seed Fund, the Maryland Momentum Fund, the University of Vermont Health Network and TEDCO.

We are currently raising Series A funding to support clinical development of VLX-1005 for HITT and advance our second drug product for treatment of Type 1 Diabetes into clinical trials. Weve initiated discussions with several large venture capital firms all of which could lead our funding round and have the full support of our current investors in the process.

What can you tell us about your experience at FITCI and as a startup in the Frederick life science ecosystem?

Ive had experiences with other incubators, some of which no longer exist, but theres no comparison to FITCI. They offer great support to emerging companies that desperately need it at the early stages. I have been at other incubators that give you a physical place to do business, but FITCI really keeps an eye on you. The FITCI team helps you solve problems and they offer quarterly meetings for the CEOs to meet with groups of successful business people who can offer advice and provide mentorship for those in need. These mentors might not be in therapeutics but theyve done this before and can really help.

I really love Frederick because, to me, the area is just like a startup. Its really going somewhere. FITCI has two locations, but whenever we meet with people, we use the Market Street location in downtown Frederick. Its a nice face to show off to people from outside of the area. Our time at FITCI is nearing its end because of our funding success, but when we graduate from the incubator, the plan is to stay in Frederick. Weve already been looking at a few places.

What are some near term challenges for Veralox and where do you see the company being in three to five years?

Our biggest challenge is developing a completely novel first-in-class product. Theres no blueprint or recipe one can exactly follow, and it is challenging. This is, however, what the Veralox team is trained to do and we are well prepared and excited by the challenge and promise of developing a new treatment that can drastically improve and perhaps save the lives of people suffering from a terrible disease.

Were also currently looking to hire a Chief Medical Officer soon. Finding the best talent is always a challenge, but I know well be able to find the right person.

In three to five years, our goal is to have several products in the clinic and possibly an approved HIT/HITT drug on the market. Veralox has the potential to become an anchor life science company in the region. But for now, Id like Veralox to be known as the company that did what they said theyd do were community-minded and will continue to work hard to make a difference in the lives of patients with debilitating diseases.

Steve has over 20 years experience in copywriting, developing brand messaging and creating marketing strategies across a wide range of industries, including the biopharmaceutical, senior living, commercial real estate, IT and renewable energy sectors, among others. He is currently the Principal/Owner of StoryCore, a Frederick, Maryland-based content creation and execution consultancy focused on telling the unique stories of Maryland organizations.

See the original post here:

IN CONSERVATION: DR. JEFF STROVEL, CEO of VERALOX THERAPEUTICS - BioBuzz

Ever since the Human Genome Project began in the late 1980s, genetics and DNA have become topics of mass interest. The book Genome: The Autobiography of a Species in 23 chapters states that the genome is a book that wrote itself, continually adding, deleting, and amending for over four billion years.

For Dr Surendra Chikara, who has been working in the field for over 20 years now, the idea of founding Bione, a healthcare startup, was a no-brainer.

Monitoring the present coronavirus outbreak scenario in the country, we have included new parameters to our Longevity Plus kit. The new updated kit provides information about the susceptibility of a person to viruses like coronavirus, SARS-like viruses, HIV, Hepatitis C virus, etc. This could be based on an individuals genetic makeup or the patterns of living, Surendra says.

Dr Surendra, Founder of Bione

Surendra says a recent addition to the Bione Genetic test can check an individuals susceptibility to coronavirus. He adds that the platforms microbiome test, combined with its predictive analytics tools and artificial intelligence, can provide tailored recommendations to individuals to strengthen their microbiome and improve their immunity.

A research paper titled 'Evidence of gastrointestinal infection of SARS-CoV-2 revealed that 23.29 percent patients infected with SARS CoV-2 showed positive results in stool after showing negative in respiratory samples. Hence, the gut microbiome test is the only way to know when a virus is no longer in your system, Surendra says.

Surendra started his career with recombinant DNA technology and worked with Dr Gita Sharma, who had created the first r-DNA vaccine for Hepatitis-B in India.

My journey in genomics started under her support and guidance. It was the time when human genome sequencing and next-generation sequencing were starting to gain importance. We were in discussions to bring D2C technology to India, but the Indian healthcare market was not ready for direct-to-consumer genetic testing," Surendra says.

This is a huge problem that all my networks were aware of. We all know that the future of the global pharmaceutical industry lies in developing precision medicines tailored for individuals based on their genes, and clinical risk for developing a disease. Indian genetic data is highly diverse and a number of breakthroughs can happen. At Bione, we are doing our part to be part of this bigger picture of making India disease-free, Surendra says.

The different types of kits depend on the number of tests covered, and include Longevity kit, Longevity Plus Kit, and MyMicrobiome kit. The Longevity Plus kit covers over 415 parameters, including health, personalised medicine, fitness, and wellness.

The team claims that it also covers a parameter that determines specific gene variants that may contribute to enhance resistance to viruses like coronavirus, HIV, Hepatitis C, and many others.

The MyMicrobiome kit identifies and quantifies the microbiome in the gut, based on which a personalised diet is recommended.

Surendra says scientific research has shown that the gut microbiome plays an important role in the function and maintenance of our immune system. In ideal conditions, this microbiome-immune system alliance allows the initiation of protective responses against germs.

The platform also offers sample collection, with samples collected from an individuals homes. A pick-up is arranged as per your convenience by Bione. The DNA sequencing is done in a well-equipped lab by expert scientists, after which a detailed report is prepared.

Bione gXplore is a user-friendly, informative, and interactive app-based platform. On it, you can go through your report and easily understand the results of DNA analysis.

Slots with genetic or food and nutrition counsellors are provided as a free-of-cost service. The expert team of counsellors guides you to proactively plan your and your familys health and lifestyle choices.

The Bione team consists of experts from global institutions and scientists domains of genomics, genetics, bio-IT, genome informatics, quality assurance, sales, marketing, genetic/nutrition/fitness counselling. The startup has a total team size of 39 people.

The startup also runs a lab with scientists, bioinformaticians, and genetic counsellors. The team is applying for ISO 9001:2015, followed by CAP and CLIA accreditation to follow global standards.

Bione is projecting to test 20,000 to 30,000 samples in the first year of operations. Tests are priced between Rs 5,000 to Rs 20,000, with the option of paying in EMIs. Customers can choose the package based on their needs.

The startup has raised angel funding from a clutch of undisclosed investors. Gourish Singla, the Founder of blockchain startup Project Shivom has invested in Bione.

Currently, startups like The Gene Box and Hyderabad-based MapMyGenome work on providing preventive solutions based on an individuals genetic makeup.

He says the startup's high tech lab is using advanced technologies, including whole genome sequencing, while the competition is still working with array technology with limited markers.

(Edited by Kanishk Singh)

How has the coronavirus outbreak disrupted your life? and how are you dealing with it? Write to us or send us a video with subject line 'Coronavirus Disruption' to editorial@yourstory.com

Read more from the original source:

How healthtech startup Bione aims to use genetic testing in the fight against coronavirus - YourStory

Clement Chow, an assistant professor of human genetics at The University of Utah, US, tweeted last week that he was in the ICU with coronavirus. And that's when researchers who had attended a meeting with him found out about it. At a time when experts are stressing on testing and contract tracing to check community transmission, this incident reveals serious and massive gaps in America's fight against COVID-19.

"Hi guys. Have you missed me? Ive been in the ICU fighting...wait for it...Coronavirus! I am the first case at the U of U ICU! Breaking the bamboo ceiling!," tweeted Chow on March 16. He further said, "Basically had a low-grade fever for a few days then a bad cough, that turned into respiratory failure. I came in and they had to put me on high flow oxygen (3 times normal)...hence ICU."

According to a March 20 report in Nature, two dozen geneticists who had attended a meeting with him nine days earlier subsequently saw the tweet and came to know that Chow had tested positive for COVID-19. While the researchers were worried for Chow, they were also upset that this was the first they had heard about it, says the report.

The fact that we learned about this from a tweet points to a failure of our department of health. But maybe we can come together with grass-root responses, Nels Elde, also an associate professor of human genetics at The University of Utah in Salt Lake City, told Nature. He had reportedly shared a dinner plate with Chow before he was diagnosed with COVID-19.

Elde tweeted to Chow on March 16 and said, "Was going through our text messages and your decision to self-quarantine early for cold-like symptoms that you were convinced was not SARS-CoV-2 was a good one and good example for us all. Get well soon @ClementYChow."

Chow further explained that his breathing was so compromised that he could not keep his oxygen levels up even with "10L of oxygen." He said while he was the first COVID19 patient in the ICU on March 19, there are more now. "Important point: we really dont know much about his virus. Im young and not high risk, yet I am in the ICU with a very severe case," said Chow.

Another researcher who had attended the meeting with Chow described how the group from 16 states "scrambled to work out who they had spent time with since returning home from the meeting." "They were upset that four days had passed between when their colleague was hospitalized with symptoms of COVID-19 and when they found out, through Twitter, that he had the disease. Another 24 hours would pass before an email from Utahs public-health departments made it their way. Every passing minute, the virus has a chance to move to someone else," reports Nature.

Meanwhile, the researchers who learned of their exposure through Twitter are taking precautionary measures by taking their temperatures and self-quarantining themselves.

Over 33,270 cases have been reported in the US so far, and 417 have died. New York state accounts for 117 deaths currently, passing Washington state, the initial epicenter of the pandemic in the US, in the number of fatal cases.

According to experts, contact tracing is important as people in close contact with someone who is infected with a virus, such as the COVID-19 virus are at higher risk of becoming infected themselves and of potentially further infecting others.

An analysis of Singapores containment measures that were implemented to minimize disease spread, for example, shows that contact tracing contributed to the primary detection of approximately half (53%) of COVID-19 patients. The study, based on a review of the first 100 cases in Singapore, shows that the mean interval from symptom onset to isolation was 5.6 days and declined after approximately 1 month.

Singapore implemented strong surveillance and containment measures, which appear to have slowed the growth of the outbreak. The study estimated that if other countries had similar detection capacities as Singapore, the global number of imported cases detected would be 2.8 times higher than the observed current number, said the report. It added, The surveillance methods in Singapore complemented one another to identify infected persons, with the overlapping components constituting safety nets; none of the methods alone would have detected all patients.

During a media briefing on March 16, the World Health Organization (WHO) Director-general Dr Tedros Adhanom Ghebreyesus had said that while there has been a rapid escalation in social distancing measures across countries, they have not seen an urgent enough escalation in testing, isolation and contact tracing which, he said, was the backbone of the COVID-19 response. "We have a simple message for all countries: test, test, test, he had emphasized.

Dr Ghebreyesus explained that while social distancing measures can help to reduce transmission and enable health systems to cope, such measures alone would not be enough to "extinguish this pandemic." "Its the combination that makes the difference. As I keep saying, all countries must take a comprehensive approach, he said.

Continued here:

Coronavirus: Massive gap in US response revealed after scientists learn colleague tested positive through twee - MEAWW

SIOUX FALLS, S.D. Averas laboratory in Sioux Falls has been verified by the South Dakota Department of Health to perform COVID-19 testing, according to a news release.

The additional testing site will allow for the processing of up to 200 tests per day.

The Avera Institute for Human Genetics has worked closely with the governors office as well as the state health department to establish guidelines on how pending tests are processed, the release states.

The most critical and highly suspicious tests will receive priority. Result time will depend on volume, however, most test results will be able to be returned in a few days and inpatient tests that are considered urgent based on the patients condition can be returned more quickly.

So far, testing for COVID-19 has been conducted by the state health departments laboratory and Averas contract laboratory.

All test results will be sent to the state for reporting purposes. Patients with positive test results will be contacted with instructions on how to care for themselves at home, symptom management, and when to contact a health care provider if symptoms worsen.

As a public service, weve opened this article to everyone regardless of subscription status.

Go here to read the rest:

Avera announces ability to test for COVID-19 in South Dakota - The Dickinson Press

Editors note: The Salt Lake Tribune is providing readers free access to critical local stories about the coronavirus during this time of heightened concern. See more coverage here.

University of Utah experts are expressing concern about the hype surrounding two medications that President Donald Trump and state officials have held up as potential treatments for the coronavirus.

Andy Pavia, chief of pediatric infectious disease at the U., is also urging caution, noting that the nations top infectious disease expert has warned that there is no convincing evidence yet that these drugs work, only stories.

The drugs have been used for years for arthritis, psoriasis and malaria, and are available in Utah pharmacies through prescription by doctors. But Grunwald said casting the unproven medications as a potential treatment for coronavirus could incite panic buying and limit the availability of the drugs for sick patients who depend on them.

The geneticist said hes not asserting that the drugs are necessarily ineffective just that they are wholly unproved.

I am simply saying defying the principles of reviewed science has dangerous consequences, especially seen in a community that is fearful and in an environment that is susceptible to panicked behavior, said Grunwald, who is a scientist, but not a medical doctor.

The drugs have not been approved by the Food and Drug Administration for COVID-19 although Utah officials said Friday that doctors still may prescribe them for COVID-19 patients here and say evidence shows they should.

On the other hand, Pavia said medical experts dont yet have good data about whether the drugs are effective against the virus.

We need to be very cautious until we have better information. In fact, chloroquine worked in the test tube against other viruses but proved to be potentially harmful when properly studied, he said. "We hope it works, but hope is not the best way to choose safe and effective treatment.

The information that youre referring to specifically is anecdotal, Fauci told reporters. It was not done in a controlled clinical trial. So you really cant make any definitive statement about it.

Trump, standing next to Fauci, still said the federal government has ordered millions of doses. He also said the nation has nothing to lose by trying it.

During Fridays news conference, Utah officials and medical representatives were essentially saying the same things as the president.

There are responses that are equivalent to Lazarus literally the biblical Lazarus people almost dead coming back, said physician Kurt Hegmann, director of the Rocky Mountain Center for Occupational and Environmental Health at the University of Utah, about hydroxychloroquine.

Officials said they are surveying Utah pharmacies to see how much of the drugs they now have on hand and are working with other states to develop plans for distributing the drugs to areas in need.

They also cautioned doctors and pharmacists to be judicious in how they dispense the drugs for now.

Utah Senate President Stuart Adams said the news conference about the drugs was called to give worried Utahns some hope.

We need some good news. We think this is good news, the Layton Republican said. We believe theres hope in America.

Utahs state epidemiologist, Angela Dunn, said last week that a lot of scientists internationally and in the U.S. are studying medications that could help treat COVID-19. Most have involved extremely small patient groups, she noted.

Current studies about the malaria drugs specifically have been very small sample sizes one in particular was only 40 people so its difficult to extrapolate that to large population," she said. So the next step is to do studies with bigger populations to see if its effective.

The rest is here:

University of Utah experts advise caution over drugs hyped as possible coronavirus treatments - Salt Lake Tribune