Monthly Archives: June 2021

REYKJAVIK, Iceland, June 18, 2021 /PRNewswire/ -- Scientists from deCODE genetics have developed a predictor based on protein measurements in blood samples that predicts the time to all-cause death better than traditional risk factors.

In a paper published today in Communications Biology, scientists from deCODE genetics, a subsidiary of Amgen, describe how they developed predictor of how much is left of the life of a person.

Using a dataset of ~5000 protein measurements in 22,913 Icelanders, of whom 7,061 died during the study period, the scientists developed a predictor of the time to death that can outperform predictors based on multiple known risk factors. The predictor can identify the 5% at highest risk in a group of 60-80 year olds, where 88% died within ten years and the 5% at lowest risk where only 1% died within ten years.

The scientists explored how individual proteins associate with mortality and various causes of death and found most causes of death to have similar protein profiles. In particular, they found growth/differentiation factor 15 (GDF15), which has been associated with mortality and ageing before, to be an important predictor of all-cause mortality. Furthermore, they found that, on average, participants predicted at high risk of death within a short period of time had less grip strength and performed worse on an exercise tolerance test and a test of cognitive function than those predicted at lower risk.

"The predictor gives a good estimate of general health from a single blood draw," says Thjodbjorg Eiriksdottir scientist at deCODE genetics and author on the paper.

"This is pretty cool but also scary and hopefully somewhat useful", says Kari Stefansson a senior author on the paper . "This shows that our general health is reflected in the plasma proteome. Using just one blood sample per person you can easily compare large groups in a standardized way, for example, to estimate treatment effects in clinical trials."

Based in Reykjavik, Iceland, deCODE is a global leader in analyzing and understanding the human genome. Using its unique expertise in human genetics combined with growing expertise in transcriptomics and population proteomics and vast amount of phenotypic data, deCODE has discovered risk factors for dozens of common diseases and provided key insights into their pathogenesis. The purpose of understanding the genetics of disease is to use that information to create new means of diagnosing, treating and preventing disease. deCODE is a wholly-owned subsidiary of Amgen (NASDAQ: AMGN).

Contact:

Thora Kristin AsgeirsdottirPR and CommunicationsdeCODE geneticsthoraa@decode.is354 894 1909

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deCODE genetics: Predicting the probability of death - BioSpace

Reading a breathless account of an amazing new medical treatment, lured in by an exciting headline, only to discover a few paragraphs in that the findings are in rodents, can at best be annoying, and at worst raise false hopes for patients and their families. A new study, long overdue, pins down one source of this common error of omission: leaving out mice in the titles of technical articles.

A chain reaction of mangled communication is at fault.

Leaving Out the Rodents

Missing mice happen at several points in the medical news trajectory.

Failure to mention that an experiment was done on non-human animals in a technical articles title can reverberate as a news release and then echo in media reports, tweets, and memes. Or, the headline of a news release or its content can ignore the mice, even if the journal article mentions them.

In yet another scenario, the reporter can omit the rodents. Journalists are sometimes so rushed with deadlines that they may modify a news release rather than take the time to read the technical report behind it that may indeed credit the mice and rats. Another source of the error: editors who write the headlines of news articles, omitting the mention (writers rarely write the headlines).

Many science journalists get ideas from the dozens of news releases posted daily at Eurekalert.org, from institutions and companies all over the world. And some releases only mention mice a few paragraphs in or not at all.

Hype resulting from mouse-deficient headlines has bugged me for a long time. When I edit abstracts for a medical journal, one of my regular gigs, I alert authors who leave out model organisms from article titles.

So I was happy to read, ironically in a news release, that Marcia Triunfol at Humane Society International in Washington, DC and Fabio Gouveia at the Oswaldo Cruz Foundation in Rio de Janeiro have investigated whether mention of mice in news release headlines dampens media coverage.

The findings described in Whats not in the news headlines or titles of Alzheimer disease articles? #InMice, published in PLOS Biology, arent surprising: when a scientific papers title omits the rodent connection, journalists reporting on the paper tend to do the same. And reporters are more likely to cover papers without mice in their titles.

Id never pitch an idea based only on mouse work to Medscape or MedPage Today, whose readers are clinicians. And I dont include such studies in my human genetics textbook.

A Mouse Isnt a Little Human

Mice are terrific models of some human diseases. Their anatomical, physiological, and genomic similarities to us make them useful in preclinical studies emphasis on the PRE.

Testing a new treatment in mice is great for amassing large numbers, implementing several control groups, and doing things that one wouldnt or couldnt do to people, like yanking out a liver or slicing up a brain to study effects of a drug. Mice in particular are useful for studying aging, collapsing the timeframe of a lifetime from 80 years to 2.

For some diseases, exploring treatments first in a model organism makes sense. But the differences among species must be considered to jump from preclinical study to clinical trial. The correspondence can come down to a single gene. According to Why Mouse Matters at the NIHs Genome.gov, on average, the protein-coding regions of the mouse and human genomes are 85 percent identical; some genes are 99 percent identical while others are only 60 percent identical.

Evolution has conserved large swathes of mammalian genomes. We use versions of the same molecules for the same things. But even when human genes are swapped into or added to rodent or monkey genomes, creating humanized creatures, differences in development impinge upon the extrapolation and interpretation of experimental results. This is particularly true for syndromes that unfurl according to a distinctive timetable, like genetic diseases with characteristic developmental delays or loss of milestones, and common chronic diseases that emerge and worsen over a lifetime, like diabetes and cardiovascular disease.

The imperfection of animal models isnt a new idea.

A study of studies from 2005, Of Mice and Men, by Lloyd Demetrius, published in EMBO Reports, has a one-sentence abstract: When it comes to studying ageing and the means to slow it down, mice are not just small humans.

Demetrius examined the misplaced use of rodents in investigating aging and caloric restriction the idea that near-starvation extends life. Theres evidence for the connection if youre a rat. For people, not so much, although reducing eating may lower weight and blood pressure and cholesterol and glucose levels in the blood, which lowers risk of chronic conditions. He argued that the different developmental timetables of rodents and us reflect differences in the aging process itself, specifically metabolic responses to stress.

So you cant extrapolate from mice living longer on a kale diet compared to littermates eating regular grub, to people making different dietary choices.

Considering Alzheimers

The new study probes the effect on media coverage of including, or not including, in mice in the title of a technical report about Alzheimers disease. They chose Alzheimers because its an exclusively human condition, but for which hundreds of mouse models have been developed to probe specific physiological responses not related to the passage of time.

The investigators divided 623 scientific reports published in 2018 and 2019 that used mice in Alzheimers disease research into those that outed the rodents in the title and those that didnt. Then they tracked the news stories appearing in the wake of publication of each study.

The papers that left out mice received more media coverage and were significantly more highly tweeted. The authors expressed concern at the misleading of the public, even if unintentional.

Most people only read the headlines of news stories. If the headline omits that the Alzheimers study was done in mice, most keep the impression that the study findings apply to humans, which is not true. We now know that virtually all findings obtained in animal studies in Alzheimers disease do not replicate to humans, said Triunfol in the news release.

Alzheimers is only one example, but the failure to identify model organisms is pervasive and a practice not likely to fade away anytime soon. In fact, when I saw the news release that inspired this post, on EurekAlert, I read another, guilty of the mouse sin: Plant-based diet protects from hypertension, preeclampsia.

But heres the first two sentences: A plant-based diet appears to afford significant protection to rats bred to become hypertensive on a high-salt diet, scientists report. When the rats become pregnant, the whole grain diet also protects the mothers and their offspring from deadly preeclampsia.

Will that headline alone trickle into news reports? Inspire tweets or Facebook memes? Probably. But the example of hypertension is less disturbing than Alzheimers blood pressure is controllable in many ways, altering diet among them.

Headlines and news reports sensationalized, perhaps inadvertently, by errors of omission, will continue. So its up to readers to realize that dramatic claims of medical advances might not apply to people caveat emptor.

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Tracing the Origins of Medical Media Hype: Failing to Mention Mice - DNA Science - PLoS Blogs

Dr. Deon Miles 97 has been a member of the faculty at Sewanee, the University of the South, since 2002, where his current course offerings include Instrumental Analysis, General Chemistry, Advanced Topics in Analytical Chemistry, Solution and Solid-State Chemistry, and the Science of Food and Cooking.

He talks about teaching, his experiences in the classroom and lab, and his path from Gary, Indiana, to a tenured professorship atop the Cumberland Plateau.

Q: Were you always interested in chemistry?

Miles: No, and its probably a story that a lot of students have. I started out to be a doctor and intended to be a biology major. The class that got me out of the biology track was genetics. I really did not enjoy it. At the same time during my sophomore year, I was taking a chemistry class, and found that material to be more interesting. I always had a love for math and science. Those two fields merged well in chemistry. The challenge in starting a chemistry major my sophomore year was how to get it done. Thankfully, the professors were very helpful in navigating that, especially Dr. (David) Phillips, and I got it done in three years.

Q: As you departed Wabash 1997, did you feel prepared for graduate school?

DM: The time at Wabash was really important. Learning how to study, not only with peers, but also on my own, to develop that hunger for knowledge, to develop those problem-solving skills, was essential. Those skills werent fully developed on day one. The molding, all that experience, helped get me to where I was ready and prepared for graduate school.

Q: What was the fall 2020 semester like for you? How did you deal with labs and the normal teaching responsibilities?

DM: I saw COVID-19 as more of an opportunity. One of the things that I did in preparation for my analytical chemistry course was to make sure students could still get a lab experience, regardless of where they were. You can record lectures, but it was the hands-on lab I was most concerned about. What I did starting in April 2020 was ask, How can we design a laboratory experience that a student can do right in their home kitchen? How can we give them an analytical chemistry experience in their homes, and do it safely? I tried very carefully to think about the kind of big picture experiments and concepts we could cover safely. We ended up coming up with seven experiments that could be done at home, and then adding three dry lab experiences things that didnt need reagents or equipment. Once finished, you then could dump them down the drain or throw things in the trash. We called them Lab in a Box. We actually used these in the labs when the students returned.

I also flipped my classroom. We didnt know if we would have students that would have to quarantine for two weeks, so I wondered how they would get the lecture content? I redesigned and recorded all my lectures, putting them in more digestible chunks. I did that throughout the semester. It was a good experience. Im going to continue to do that kind of going forward because it gives me the opportunity to do more things in class that I didnt have the opportunity to do before because of the lecture content.

Q: Did you find it harder to engage with your students?

DM: There were moments, yes, when it was more challenging to stay engaged with the students. Thankfully, all my students this past semester were in person. Because I flipped the classroom, I would come in and ask if there were any questions. A lot of times there were, but there were times I didnt have another activity planned, so we would meet, go over questions, and 10-15 minutes later, we were leaving.

We were so focused on physical distancing and not spending a lot of time together. All those informal interactions went away. Those informal interactions are the things I missed the most.

Q: Did you hear from your students about mental health concerns, or perhaps sense moments where questions unrelated to chemistry might alleviate some stress?

DM: Those moments happened one-on-one. Im in my 19th year as a professor. I can see when a student wants to have that kind of conversation. They put their things away slowly, they linger a little bit. Everybody else is running out of the class. I had opportunities to ask, how are things going? A student might have needed a couple of more days to do a lab report after staring at the same four walls for the last three days. We recognized that and we got through the semester.

Q: Did some of those informal conversations and the questions that were on students minds outside of class allow you to talk of chemistry in timely, topical, or different ways?

DM: When we think about chemistry, we dont necessarily think about social justice. Its almost like, just stick with atoms and molecules and then move on. But thats not entirely true. Ive tried to lead by example and have started to incorporate some aspects of social justice in my classes. When you think about social justice and think about this from a chemistry perspective, its about getting students to think beyond their immediate circles of influence. How do you do that with chemistry?

The water crisis in Flint, Michigan, is a great example. What happened with the lead pipes? How did the water get lead in it? From an analytical chemistry perspective, we can talk about the instruments that are used to detect the lead. We can also talk about the human side of it. We can talk about the impact of lead water on children under the age of six and how it slows development in a number of ways. Thats one way analytical chemistry can enter into conversations about social change. I want my colleagues to find more examples and see how we can incorporate those into our courses. We still get the chemistry, but lets think about the human aspect as well.

For more stories about alumni making a difference in education, check out the upcoming issue of the Wabash Magazine, available in early July.

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Deon Miles '97: Think About the Human Aspect - Wabash College

Its estimated 150 million Americans 57 per cent of the country watched the verdict in the 1995 OJ Simpson trial.

The case dominated news bulletins around the world and in the stand as an expert witness was Kiwi mathematician Bruce Weir.

For three days, the world-renowned authority on biostatistics discussed the blood samples taken from Simpsons car and glove. The DNA evidence was overwhelming ... and it all pointed in the same direction, he says.

He faced a grilling from Simpsons lawyer, and at one stage conceded an error in his calculations. Having spent months working on the complex equations with a colleague, he was asked by the judge to provide additional data.

I went back to my hotel room and did them overnight. I left out one term, so the numbers were not correct. Unfortunately for me, and maybe fortunately for the defence, they spotted this. I dont think it was a crucial element.

Simpson was found not guilty, and the extensive media coverage of the trial made Weir a recognisable figure on American streets. I couldnt go anywhere without being recognised. When you are on national TV for an extended period you get known.

The 77-year-old now lives and works on Americas northwest coast, 11,000 kilometres from where he grew up in Christchurch.

Last month he became a Fellow of the Royal Society, the oldest and most prestigious national scientific institution in the world.

READ MORE:* Fifty years of asteroid hunting for Kiwi couple* National Portrait: Antarctic archaeologist Dr David Harrowfield * Poet and writer Mohamed Hassan on searching for home* New headmaster chosen for Christchurch's Shirley Boys' High School

Its a huge honour, he says, but he feels most proud to be one of the 50 or so New Zealanders who have been elected.

Lord Rutherford and a couple of Nobel Prize winners. I don't even think of being at that level, but it's nice to be in a group which has those.

Biostatistics is an area of expertise that has played a vital role in the fight against Covid-19.

Data analysis was used during the clinical trials for the coronavirus vaccines and to study mutations in the virus, he says.

When there's an outbreak they can see which variant and where it came from. It's the numbers which are so crucial.

And he praises New Zealands response to the pandemic, especially the sequencing, which has been world class.

Born in 1943, Weir was raised in the Christchurch suburb of Shirley with his four siblings.

Most of his family worked in the trades and his dad hoped he would become a plumber.

My father worked in a factory, he rose through the hierarchy, but he worked with his hands, Weir says.

My mother had been secretarial and that was typical for our family. My aunts and uncles all had good jobs but not what we'd call professionals.

Supplied

Shirley Boys' High School headmaster Charles Gallagher with First-Day third formers Trevor Purver, Neville Burnby, Peter Cox, Robert Clarke, Grant Webley, and Robert Dollan. Image taken around 1957.

In November 1957, Shirley Boys High School opened and Weir was one of 156 form three students, now known as First-Day Pupils.

He remembers it being an exciting time.

It was a brand new school, new building, new staff who were very enthusiastic.

I was one of the boys who got to unpack the chemistry equipment, and I'd never seen a test tube or a beaker. It was a whole new world.

Nearby Christchurch Boys' High was founded in 1881 and a healthy rivalry was quickly established between the two schools.

We were on a mission, he says. We were the second public boys' school and we had a rival. There was also the other private boys' schools, Christ's College, St Andrews, St Bedes, and we tried very hard to be part of that scene.

Weirs time at Shirley Boys was instrumental, especially the guidance he received from the amazing headmaster Charles Gallagher, who helped him launch his academic career.

Supplied

Shirley Boys' High School. Back L-R Graeme Hern, Cyril Morris, Ross Nicholas Front L-R Alex Wilson, Max Wright, Headteacher Charles Gallagher, James Barrie and Bruce Weir. Image taken in 1959.

His degree was in maths and he was personally very encouraging.

Weir was made head boy and in 1961 became the schools first dux.

But despite the plaudits, the following week he was working a summer job on the rubbish trucks.

I got all the prizes and then a week later I was on D and R dust and rubbish.

After winning a scholarship, he attended the University of Canterbury (UC), the first of his family to go to university.

It was a bit daunting. It was hard work, but that was fine.

Whilst at UC he began an internship at the Department of Scientific and Industrial Research under acclaimed statistician Brian Hayman, who worked in genetics.

I had no idea what genetics was, Weir says.

Hayman told him to read Genetics by biologist Hans Kalmus and the book sparked an interest that would shape his career.

I read that and thought wow. Who knew we had genes and they seem to obey some mathematical rules? I thought that was neat.

At that point, genetics was largely concerned with plants and animals and most statistical work was used for improving crop or milk yield, he says.

After graduating in 1965 with a first class degree in mathematics, Weir undertook a PhD in statistics with a minor in genetics at North Carolina State University, in the US.

There he met Columbus Clark Cockerham who developed the language for statistical genetic data and the pair would undertake pioneering work over the next three decades.

During his post-doctoral studies in California in the late 1960s, Weir was part of a team that studied human genes a field which was still in its infancy.

We were so excited, we had information on four genes, this was unprecedented. In the work I'm doing now, we have a billion.

He returned to New Zealand in 1970, working as a senior lecturer at Massey University.

And he could be seen driving around Palmerston North in a 1966 Ford Mustang, which he shipped back from America.

In those days you couldn't travel to the US by air, unless you were extremely rich, so everybody sailed.

Coming back, my checked luggage was my Mustang.

Supplied

Bruce and Beth Weir's wedding in August 1971. The couple drove away in his 1966 Ford Mustang.

While at Massey he met his wife Elizabeth Swainson, his American car having caught her eye.

I think it helped attract my wife. We sold it at a huge profit and it helped us buy our first house.

The couple would have two children together, Claudia and Henry, and in 1976 they moved to the States, with Weir becoming the founding director of the Bioinformatics Research Centre at North Carolina State University.

Today, he is an honorary professor at the University of Aucklands Department of Statistics but is primarily based in Seattle, where he is a professor of biostatistics, epidemiology and genome sciences at the University of Washington Schools of Public Health and Medicine.

As a lecturer, he has been prolific supervising more than 35 PhD students but he is best known for his groundbreaking research.

The book he co-wrote on interpreting DNA evidence is considered the definitive text for lawyers and judges.

And his biostatistical studies have resulted in the publication of more than 200 peer-reviewed articles.

By the early 1990s, DNA profiling was increasingly being used in criminal investigations and Weir was approached by the FBI to help ensure its calculations were rigorous.

He provided testimonies in about 20 trials, before prosecutors in Los Angeles County asked him to assist in the trial of Simpson,

the American actor and former NFL player who was arrested and charged in 1994 with the murders of his ex-wife Nicole Brown Simpson and her friend Ron Goldman.

Reed Saxon/AP

OJ Simpson and defence attorney F. Lee Bailey during the double murder trial in Los Angeles on June 30, 1995.

Though he was acquitted, he would later serve nine years for a robbery-kidnapping conviction in Las Vegas.

Weir hopes his own work will one day lead to cures for a range of illnesses.

Conditions like Alzheimer's disease could be better treated with the identification of what gene causes it.

We could then maybe give the person a drug to compensate for what that person's gene was not doing. It all rests on the data.

Supplied

Bruce and Beth Weir (centre). Their daughter Claudia Weir and son Henry Weir, with his children Zoe and Spencer.

In May, Weir became a Fellow of the Royal Society, which was founded in 1660 and is made up of the most eminent scientists, engineers and technologists from throughout the Commonwealth.

He was recognised for his contributions to the theory of population and quantitative genetics and to forensic science.

Each year 52 new Fellows are elected and for the 2021 elections there were almost 700 candidates.

Current members include around 75 Nobel Prize winners, while past Fellows include Isaac Newton, Charles Darwin and Alan Turing.

Weir says its a huge honour but he feels most proud to be one of the 50 or so New Zealanders who have been elected.

Lord Rutherford and a couple of Nobel Prize winners. I don't even think of being at that level, but it's nice to be in a group which has those.

One of the things he is especially delighted about is that his election means Shirley Boys' High School now has a fellow of the Royal Society.

We have joined Christ's College and Christchurch Boys'. Thats a big deal.

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National Portrait: New Royal Society fellow Bruce Weir on DNA and that OJ Simpson trial - Stuff.co.nz

Special purpose acquisition companies (SPACs) have been the talk of Wall Street for more than a year now. And although 2020 was deemed the year of the SPAC, 2021 also has welcomed a few of their own. That said, business mogul Richard Branson and 23andMe are getting in on the action.

Source: Sergei Bachlakov / Shutterstock.com

What do these two have going on, and why should investors care?

Lets dive in and take a closer look at the latest SPAC move featuring Richard Branson and 23andMe.

Shares of VGAC stock rose nearly 10% the day of the announcement but are down about 4.7% as of Tuesday afternoon.

On the date of publication, Nick Clarkson did not have (either directly or indirectly) any positions in the securities mentioned in this article.

Nick Clarkson is a web editor at InvestorPlace.

Article printed from InvestorPlace Media, https://investorplace.com/2021/06/vgac-stock-everything-you-need-to-know-about-richard-branson-23andme-and-this-weeks-spac-merger/.

2021 InvestorPlace Media, LLC

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VGAC Stock: Everything You Need to Know About Richard Branson, 23andMe and This Week's SPAC Merger - InvestorPlace

In June 2020, as the first reports of long Covid began to filter through the medical community, doctors attempting to grapple with this mysterious malaise began to notice an unusual trend. While acute cases of Covid-19 particularly those hospitalised with the disease tended to be mostly male and over 50, long Covid sufferers were, by contrast, both relatively young and overwhelmingly female.

Early reports of long Covid at a Paris hospital between May and July 2020 suggested that the average age was around 40, and women afflicted by the longer-term effects of Covid-19 outnumbered men by four to one.

Over the past 12 months, a similar gender skew has become apparent around the world. From long Covid patients monitored by hospitals in Bangladesh and Russia to the Covid Symptom Tracker app, from the UK-wide Phosp-Covid study assessing the longer-term impact of Covid-19, to the medical notes of specialist post-Covid care clinics across both the US and the UK, a picture has steadily emerged of young to middle-aged women being disproportionately vulnerable.

Dr Sarah Jolley, who runs the UCHealth post-Covid care clinic in Aurora, Colorado, told the Observer that about 60% of her patients have been women. In Sweden, Karolinska Institute researcher Dr Petter Brodin, who leads the long Covid arm of the Covid Human Genetic Effort global consortium, suspects that the overall proportion of female long Covid patients may be even higher, potentially 70-80%.

This pattern has been seen in other post-infectious syndromes, says Dr Melissa Heightman, who runs the UCLH post-Covid care clinic in north London. Around 66% of our patients have been women. A lot of them were in full-time jobs, have young children, and now more than a quarter of them are completely unable to work because theyre so unwell. Economically, its a bit of a catastrophe.

As Heightman points out, this is not a new trend when it comes to infectious diseases, rather one which has historically been neglected. Women are known to be up to four times more likely to get ME/CFS (myalgic encephalomyelitis, or chronic fatigue syndrome), a condition believed to have infectious origins in the majority of cases, while studies have also shown that patients with chronic Lyme disease are significantly more likely to be female.

But despite this, there have been relatively few attempts to drill down into why this is the case. Instead, because these conditions predominantly affect women, they have more often been dismissed as being psychological in origin. Over the years, both ME/CFS and chronic Lyme disease have been ridiculed by sectors of the medical community as forms of hypochondria.

In general, theres not as much research money and attention on conditions that primarily affect women, says Julie Nusbaum, an assistant professor at NYU Long Island School of Medicine. Thats just a general disparity in medical research. I think certain biases persist that when women present with a lot of body aches or pains, theres more often an emotional or personality component to it than medical origin.

Worryingly, signs of these age-old biases have crept in over the past year with long Covid. There are anecdotal reports of female patients complaining that their persistent symptoms have been dismissed or attributed to anxiety. Dr Janet Scott, an infectious diseases specialist at the University of Glasgow, says that there remains a school of thought within the academic community that the long Covid gender skew may simply be an artefact of women being more likely to report symptoms than men.

I dont buy it myself, says Scott. I think it plays into the narrative of, Dont worry about long Covid, its just a bunch of hysterical, middle-aged women.

But Scott and other scientists around the world are trying to delve into the different factors which make women more prone to developing long Covid. Understanding them could be crucial to shedding a light on this mysterious condition in general, as well as other illnesses which can be triggered by an infection.

At Yale School of Medicine, Connecticut, immunologist Prof Akiko Iwasaki has spent much of the past year trying to tease apart the differences between how men and women respond to the Sars-CoV-2 virus. One of her early findings was that T cells a group of cells important to the immune system which seek out and destroy virus-infected cells are much more active in women than men in the early stages of infection. One component of this is thought to be due to genetics.

Women have two copies of the X chromosome, says Iwasaki. And many of the genes that code for various parts of the immune system are located on that chromosome, which means different immune responses are expressed more strongly in women.

But it is also linked to a theory called the pregnancy compensation hypothesis, which suggests that women of reproductive age have more reactive immune responses to the presence of a pathogen, because their immune systems have evolved to support the heightened need for protection during pregnancy.

This robust immune response is thought to be one of the reasons why women are much less likely to die from Covid-19 during the acute phase of the infection but it comes with a catch. One of the major theories for long Covid is that fragments of the virus manage to linger in remote pockets of the body, known as reservoirs, for many months. Iwasaki says that remnants of Sars-CoV-2 have been discovered in almost every tissue from the brain to the kidneys.

Because women react so strongly to the presence of a virus, some scientists think that these viral reservoirs are more likely to trigger waves of chronic inflammation throughout the body, leading to the symptoms of pain, fatigue and brain fog experienced by many with long Covid.

Evidence to support this idea has been found in studies of chronic Lyme disease. The bacterium Borrelia burgdorferi, which causes Lyme disease, is also capable of burrowing into tissue and nerves and hiding out in the body, leading to chronic symptoms. Research has shown that women have a more intense response to the presence of B burgdorferi, producing much higher levels of inflammatory cytokines small proteins than men.

Theres increasing evidence that women respond more to this kind of persistent, low-grade infection than men, says Dr Raphael Stricker, a Lyme disease researcher based in San Francisco. And so theyre much more likely to have chronic inflammation.

This is unlikely to be the sole explanation, however. Many scientists studying long Covid believe that, in a proportion of cases, the virus may have triggered an autoimmune disease, causing elements of the immune system to produce self-directed antibodies known as autoantibodies, which attack the bodys own organs. Since December last year, Iwasaki and others have published studies that have identified elevated levels of more than 100 different autoantibodies in Covid-19 patients, directed against a range of tissues from the lining of blood vessels to the brain. While the level of some of these autoantibodies subsided naturally over time, others lingered. Iwasaki believes that if these self-directed antibodies remain in the blood of long Covid patients over the course of many months, it could explain many of the common symptoms, from cognitive dysfunction to clots, and dysautonomia a condition where patients experience an uncomfortable and rapid increase in heartbeat when attempting any kind of activity.

There have previously been indications of this in studies of ME/CFS. Female patients have been found to be far more likely to experience autoimmune-related ailments, ranging from new allergies to muscle stiffness and joint pain, a similar symptom profile to many of those with long Covid.

Iwasaki is now conducting another study looking to examine whether certain autoantibodies are present in particularly high levels in female long Covid patients. If this proves to be the case, it would not come as a complete surprise. Viruses have long been linked to the onset of autoimmune diseases ranging from type 1 diabetes to rheumatoid arthritis, and all of these conditions are far more prevalent in women, with surveys finding that women comprise 78% of autoimmune disease cases in the US.

Viral infections prompt the immune system to respond, says Nusbaum at NYU. And for many women, particularly if theyre genetically predisposed, that immune response can be so robust that you enter into this kind of dysregulated immunity, which doesnt get turned off even after the virus is cleared.

Women are more prone to autoimmune problems for a number of reasons, ranging from a molecular switch called VGLL3, which women have in far higher levels than men and which can tip the immune system into overdrive, to the sex hormone oestrogen, which can increase inflammation. Men on the other hand are more protected against developing autoimmune-related problems due to their higher levels of testosterone, which suppress the number of autoantibody-producing cells called B cells. Iwasaki believes that this tendency may well be the major factor that explains the long Covid gender skew.

In the case of long Covid, the virus may tip the balance towards autoimmunity in people who already have that tendency to begin with, she says.

Some scientists have already begun to describe long Covid as an oestrogen-associated autoimmune disease, calling for more research dedicated to identifying both personalised and gender-specific long Covid treatments.

If autoantibodies are consistently found in particularly high levels in female long Covid patients, one approach could be to treat them with immunosuppressive medications, such as steroids.

We need to try and identify the underlying causes in each case, says Iwasaki. That could be one approach, while in other cases where the problem is a persistent Covid-19 infection, you might want to treat those patients with antivirals. Well continue to get more information on this over the next few months.

Many hope that the answers gleaned from understanding the long Covid gender skew could also help provide more insights into treating other conditions that are particularly prevalent in women, such as ME/CFS, and even certain autoimmune illnesses.

A lot of the symptoms being experienced by the Covid long haulers are very similar to chronic fatigue syndrome, fibromyalgia and some of these other chronic conditions that we dont fully understand, says Nusbaum. I do think its possible that the attention now being placed on long Covid could help provide an insight into that, which would be a very welcome benefit.

Read more:
Why are women more prone to long Covid? - The Guardian