More than a year after his murder, ‘Jordan’s Law’ heads to the governor’s desk – WTSP.com

LARGO, Fla. "Jordan's Law," initially introduced by State Rep. Chris Latvala (R-Clearwater) is making its way to Gov. Ron DeSantis desk for his signature.

The bill passed unanimously 113-0 Thursday afternoon in the Florida House and 40-0 earlier this month in the Florida Senate.

Last year, the bill designed to protect children from abuse did not make it through the Senate. Sources told 10Investigates at the time senators would not hear the bill because of legal issues in the way the bill was written.

But several lawmakers refused to give up.

State Representatives Chris Latvala, Ben Diamond, Jennifer Webb, state senators Darryl Rouson, Ed Hooper re-introduced Jordans Law for the 2020 legislative season.

The bill is set to accomplish the three following items to better protect children in the states child welfare system:

Jordan Belliveau went missing in September 2018 and police issued an AMBER Alert. His body was later found in the woods.

Proscutors say his mother, Charisse Stinson, lied about his disappearance. She is facing first degree murder, aggravated child abuse and providing false information to a law enforcement agent during an investigation charges.

Her trial is currently set to start on Aug. 10, 2020.

Click hereto read the bill.

RELATED: Thousands want new law passed a year after prosecutors say this toddler was murdered by his mom

RELATED: Florida lawmakers plan to reintroduce 'Jordan's Law' after Largo toddler's death

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More than a year after his murder, 'Jordan's Law' heads to the governor's desk - WTSP.com

Detailed Look At Melody Ehsanis Cherry-Clad Take On The Womens Air Jordan OG – Sneaker News

Melody Ehsanis relationship with Jordan Brand, though young, has amassed quite a bit of rapport with the sneaker world at large her previous FEARLESS Air Jordan 1 continuing to rise up the resell charts. Now, with arguably the same level of energy, the burgeoning designer has diverted her sights to the OG womens Air Jordan silhouette, using its relatively unembellished constructions to celebrate womens history month, the icons of the WNBA, and the Love & Basketball anniversary. Simple and marked by only a two-toned palette, the pair outfits primarily with black shades, accents arriving atop with reflective piping at the edge of the overlays and vibrant reds at both the lining, tread, and branded heel embroidery. Elsewhere, other than the ME adorned box, is kept sound with little in the way of changes, but as cherry themes are interwoven throughout, the kit will finish by way of a playful and idealistic emblem of the fruit at the vamp in place of a dubrae. Grab an official look at these right here and expect a release first at the womenswear labels Fairfax and Soho locations on March 14th; a global launch will then follows shortly after on March 19th.

In other news, the Jordan Westbrook One Take was revealed in another colorway.

Melody Ehsani x Womens Air JordanME Release Date: March 14th, 2020Global Release Date: March 19th, 2020Color: Black/Infrared/Hyper GrapeStyle Code: CQ2514-005

Make sure to follow @kicksfinder for live tweets during the release date.

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Detailed Look At Melody Ehsanis Cherry-Clad Take On The Womens Air Jordan OG - Sneaker News

First Look At The Air Jordan 4 Rasta – Sneaker News

After the Bred 4s drop not too long ago, the silhouette has been relatively under wraps, only hitting the spotlight afterwards thanks to its runway relationship with Virgil Abloh. Inciting exciting for its inevitable Fall/Winter release, the collaborative silhouette has opened up audiences to newfound Air Jordan 4 GRs this latest bearing a Rasta inspiration and an exclusive womens size run. Hued primarily in white, coupled with standard leather fixtures, the pair plays to its themes with a punchy though sparing use of color, preferring to distinguish itself by way of variety alone. As such, heritage palettes of orange, yellow, and green create a slight gradient across the cages that hit the vamp and side; elsewhere, treads and lining are dyed a green to match and the attached hang tag breaks up in bright red as it hangs just below black-dyed eye stays and laces. Grab a detailed look here and expect a release to arrive later this April if COVID-19 doesnt create further delays.

In related news, an Air Jordan 4 Court Purple was just revealed in detail.

Air Jordan 4 RastaRelease Date: April 2020$190Style Code: AQ9129-100

Source: @hanzuying

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Official Images Of The Air Jordan 4 Retro SE Neon – Sneaker News

Amid news of several Jordan release date delays, The Jumpman Brand has revealed official images of the Air Jordan 4 in its best Air Max 95 impression.

Slated to drop in a weeks time, the latest iteration of Michael Jordans fourth signature shoe is a complete departure from its most recent counterparts, as well as the upcoming Off White Jordan 4. From midsole to tongue, the upcoming retro stacks various shades of grey on-top of one another to resemble the aforementioned Air Max runner, which is celebrating its 25th Anniversary. Elsewhere, plastic eyestays, profile mesh guards and tongue labels all contribute to the Jordan 4s nod to its kin from 95: Volt animates the four plastic lace guards and half of the tongue patch, while surrounding netting keeps things subtle like its muse. And while previous leaks revealed other distinct nods to the 25-year-old silhouette at the Airbag, insole and outsole, official images are the first to demonstrate one of the Air Max 95s most signature details: A reflective NIKE AIR-branded spine.

The Jordan 4 Neon is scheduled to launch at Nike.com on March 21st in Pre School, Grade School and Adult sizing. Pricing for this pair will range from $80 USD to $225 USD.

In other 2020 Jordan Releases news, official release details for the womens Melody Eshani Jordan have emerged.

Air Jordan 4 Retro SE NeonRelease Date: March 21st, 2020$225Color: Cool Grey/Volt/Wolf Grey/AnthraciteStyle Code: CT5342-007 (Adult)Style Code: CT5343-007 (Grade School)Style Code: CT5345-007 (Pre School)

Make sure to follow @kicksfinder for live tweets during the release date.

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Official Images Of The Air Jordan 4 Retro SE Neon - Sneaker News

The Air Jordan 1 Mid Is Covered In Patent Leather Pastels And More – Sneaker News

Whether you hate or simply tolerate the Air Jordan 1 Mid, theres no denying that its here to stay, and if the past month is any indication, then its likely the brand is going to continue ramping up the release cadence gradually with time. The models latest, which removes the ostensibly trending basketball leathers, opts for a material treatment far more familiar with its overlays of shiny patent, directly applying them to both the forefoot as well as the heel counter in black and pink, respectively. The latter, though bright, is still not the brightest color amongst the palette, surprisingly, as the swooshes along both the lateral and medial mismatch with shades of neon green and aqua blue. Elsewhere, the pair is left neutral in its base of white and accents of its darker tonal opposite. Grab a detailed look at these Mids here and expect a release at Nike.com soon.

In other Jumpman news, the Jordan React Delta has just been revealed in full.

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The Air Jordan 1 Mid Is Covered In Patent Leather Pastels And More - Sneaker News

Where To Buy The Air Jordan 1 High Zoom Racer Blue – Sneaker News

First teased shortly after December 2019s Fearless Ones release, the second Air Jordan 1 Zoom is finally dropping on March 14th. While Michael Jordans first signature shoe has previously been reimagined for both accessibility and fashion purposes (see: Jordan 1 Flyease, Jordan 1 Jester), its Zoom-cushioned version proffers responsiveness never-before-seen on the classic model.

Clad in Pure Platinum/White, this pair keeps the 85-icons tall silhouette, but features a few notable updates. Transparent ankle flaps don printed ball-and-wings insignias and sit atop lateral ZOOM-branded tabs. Further denoting its use of NIKE, Inc.s big bet for 2020, this Jordan 1 exchanges standard NIKE AIR tongue labels for ZOOM AIR equivalents. Elsewhere, the Dior Jordan 1-like option breathes new life into the 35-year-old design via the colorful gradient visible through its icy outsoles.

The Jordan 1 Zoom Racer Blue hits Nike SNKRS on March 14th for $175 USD. While you wait, enjoy another look at this pair here below and bookmark our Jordan Release Dates For 2020 calendar.

If you prefer performance-basketball options, Zion Wiliamsons Bayou Boys Jordans PE is hitting retailers on March 13th.

Air Jordan 1 High Zoom Racer BlueRelease Date: March 14th$175Color: Pure Platinum/Racer Blue/WhiteStyle Code: CK6637-104

Make sure to follow @kicksfinder for live tweets during the release date.

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What Happened to Jordan Peterson? – The New Republic

So far, there is no evidence that Peterson displayed any of the so-called aberrant behaviors that define addiction. Butagain, all we have to go on is reports from his daughter, whose family has astrong financial incentive to spin away any suggestion that the man who madehis name engaging in a kind of intellectual Spartan cosplay is hopelesslyaddicted to a sedative. In fact, Mikhaila has jokingly alluded to how bad anaddiction diagnosis would be for her fathers lucrative self-help brand, whichpurports to rid adherents of weakness through grit and self-sacrifice. Wefigured we should let people know [the facts] before some tabloid finds out andpublishes [that] Jordan Peterson, self help guru, is on meth or something,Mikhaila said in a video update after Peterson checked himself into rehab inthe U.S.

Still, as soon as Petersons initial stint inrehab became public in 2019, threads sprang up in Peterson-related forums aboutwhether his fans should think less of him in light of his struggles with benzodiazepines.He was using a drug to escape the pain of reality, period. Call it whateveryou like, but it doesnt change the facts, wrote the user KingLudwigII on Reddit. In fact, dependence and addiction arehealth issues, not character defects, and if you pressed Peterson on thatpoint, hed probably agree. However, that message is a tough sell to many ofPetersons fans, who are drawn to his macho image and his personal story oftriumph over adversity.

By August or September 2019, Petersonshealth had deteriorated to the point that the family was more worried about himthan his cancer-stricken wife, Mikhaila said in an appearance onRT, the Russian propaganda network aimed at audiences outside of Russia.

There are established ways of treating adependence on benzodiazepines, a class of sedativesincluding Klonopin(clonazepam), Valium (diazepam), and Xanax (alprazolam)used for anxiety,insomnia, and epilepsy. Introduced to the U.S. market in 1960 as an alternative to barbiturates,benzodiazepines can be useful in treating a variety of conditions from panicattacks to muscle spasms. They can be very helpful for short-term andintermittent use, but their benefits tend to wanewhen they are used every day. They can also cause physical dependence within four weeks. If a person whos physicallydependent on benzodiazepines stops taking the drugs suddenly, they can sufferfrom withdrawal symptoms including severe anxiety, agitation, and evenlife-threatening seizures.

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Horace Grant goes in on the real Michael Jordan – Basketball Network

Horace Grant was one of the most underappreciated and underrated players of the 90s, providing a vital role on some pretty good teams from that era like the Chicago Bulls, Orlando Magic, and the Los Angeles Lakers.

The talented power forward was the third option behind Jordan and Pippen during the Bulls threepeat in 1991,1992, and 1993. Even after he left the Bulls, Grant was a crucial part of the rising Orlando Magic with Shaq and Penny. Being a part of the championship Bulls in the early 90s, Grant had the chance to witness the greatness of Michael Jordan and all the stories and events that occurred around him and his persona.

Grant made a guest appearance on HOT 97 for a discussion that mostly revolved about his former teammate, MJ, and all the stories that he experienced during his time with the Bulls organization. A particularly exciting piece of the interview was when Grant talked about how he and Pippen knew before the game started if they were going to win.

Scottie & I.. used to stand on the sideline when MJ went out to halfcourt. If we see the captains of the other team shake his hand & smile & laugh, we know we had that game. Because theyre having fun with MJ, but we knew MJ was thinking about putting the boot on your throat.

You could say their job was pretty easy in those games because MJ would take care of most of the work, but they all had to match his intensity to a certain degree because he couldnt do it by himself. That is just one of many examples of how Jordan was passionate and competitive since the moment he would walk into the arena.

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Cameron Jordan criticizes Jaguars for trading Calais Campbell to the Ravens – Saints Wire

The Jacksonville Jaguars agreed to a puzzling trade on Sunday, sending Pro Bowl defensive lineman Calais Campbell to the Baltimore Ravens for no more than a fifth-round draft pick. Campbell is one of a handful of players who have created 6.5 or more sacks and 50-plus tackles in each of the last three years another one is New Orleans Saints captain Cameron Jordan, who took aim at the Jaguars for jettisoning such an important piece of their defense.

Jordan lambasted the Jaguars for their lack of loyalty to Campbell; he pointed out Campbells contributions on the field and off of it in Jacksonville, and criticized them for not appreciating Campbells influence in the locker room, as the vet leader that they didnt deserve but had at (the) helm.

Its easy to see why this stings so badly for Jordan. Campbell is someone hes long admired, having watched the big defensive ends NFL career start with the Arizona Cardinals while Jordan was a student at nearby Chandler High School. They have similar styles of play and levels of production, and Jordan obviously has a lot of respect for what hes accomplished.

Fortunately, this isnt a scenario that Saints fans should have to see play out. Jordan signed a contract extension last summer that ties him to New Orleans for the foreseeable future; hes one of the best players on a team whose arrow is still trending up, towards yet another year of Super Bowl contention. While the Jaguars may be willing to sacrifice fixtures of their franchise for unclear reasons, Jordan and the Saints are very much in the business of competition.

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Cameron Jordan criticizes Jaguars for trading Calais Campbell to the Ravens - Saints Wire

Love Islands Rebecca Gormley cosies up with ex Jordan Waobikeze after going official with Biggs just last m – The Scottish Sun

LOVE Island's Rebecca Gormley cosied up to ex Jordan Waobikeze at a sports awards ceremony last night - and all in front of boyfriend Biggs Chris.

Last month The Sun Online exclusively revealed that the Geordie lass, 21, and car body repair specialist, 27, were officially dating - and their first date was at a kebab shop.

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But it looks like the beauty queen got up close and personal with her ex Jordan, 24, at the British Ethnic Diversity Awards in London last night.

The administrator, 24, took to his Instagram story to document his big night out with the some other islanders, including: Luke Trotman, 22, Siannise Fudge, 25, Mike Boateng, 24, Priscilla Anyabu, 25, and even Rebecca's beau Biggs.

In the now deleted snap the pair posed for a selfie together and Jordan placed a whispering emoji in between them and he covered his mouth with his hands.

Rebecca gave her best sultry eyed look in her red dress, smoky makeup and perfectly curled hair.

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During their time on the ITV2 reality show Jordan and Rebecca shared a kiss which led onto them coupling up together for the duration of their stay in the villa.

Jordan went on the join the girls in the main villa after the boys headed to Casa Amor - and it wasn't long before he caught the eye of Rebecca - who wasn't coupled up with anyone else.

The brunette beauty chose to keep Jordan in the main villa when the two camps were reunited after Casa Amor.

But their time on the show was short lived when they were voted the least popular couple in the villa.

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Rebecca went on to admit that she thought their romance came "to a standstill" and said:"It wasn't going anywhere. And I think if you want to be with someone things should be progressing every day, not at a standstill. It became a friendship rather than being in a romantic couple."

The Miss Newcastle 2018 went onto admit that she regretted not getting to know any of the other boys.

"I wish I did chat to them all and find out more about everyone else - like Biggs. I loved Biggs (Chris). He was mint. His personality is the kind of personality I would go for. I would definitely meet up with him," she said.

Insiders said that the beauty queen felt pressured to hook up with Jordan - despite wanting to get to know Biggs when she returned to the UK.

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After being kicked out the villa alongside Jordan, Rebecca talked about "taking things slow" as she was quizzed about their relationship by host Laura Whitmore.

But within hours she was already having second thoughts and had been spending time with Biggs since flying back to the UK.

The pair finally went official with their relationship when they were pictured outside a kebab shop in the capital.

Theytucked into a mixed doner kebab and chips and Biggs proved that he is Instagram husband material as he snapped Rebecca posed with her food for Instagram.

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"Just had my first@germandonerkebabuk & it was absolutely naughty! I will definitely be going back#kebabsdoneright#ad," she posted.

And Rebecca reciprocated as she snapped a picture of Biggs smiling with his "cheat meal".

Biggs - who is signed toThe Model Team- was one of the Casa Amor boys who got to live in the main villa for a week as he grafted for the girls.

During their time in the villa he couldn't make a move because Rebecca and Jordan had already hit it off and so he set his sights on Jess Gale.

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Love Islands Rebecca Gormley cosies up with ex Jordan Waobikeze after going official with Biggs just last m - The Scottish Sun

Michael Jordan’s Teammate Reveals What Jordan Shared Before Preseason Game in 01 – Heavy.com

After the 1998 season, Michael Jordan decided to retire from the NBA for the second time after winning his sixth and Final NBA Championship against the Utah Jazz.

Two years later, he would announce that he was back, but this time not as a player as president of basketball operations for the Washington Wizards. Jordan would have the final say on all personnel matters. Jordan was able to get rid of some large contracts such as Juwan Howard and Rod Strickland. However, In his first NBA draft as an executive, Jordan drafted Kwame Brown with the first pick of the 2001 NBA draft.

Despite his claim that he was 99.9% certain that he would never play another NBA game in January 1999, according to ESPNs Larry Schwartz. In the summer of 2001, Jordan expressed interest in making another comeback. Jordans comeback was inspired by his friend Mario Lemieux, who decided to make a comeback of his own the winter before.

The Jumpman [Michael Jordan] spent much of the spring and summer of 2001 in training, holding several invitation-only camps for NBA players in Chicago. Also, Jordan made the decision to hire his old Chicago Bulls head coach,Doug Collins, as Washingtons coach for the upcoming season. It was a move that foreshadowed Jordan returned to the NBA.

Jordan would announceon September 25, 2001, that he be returning to the NBA to play for the Washington Wizards. He also announced that he would be donating his salary as a player to a relief effort for the victims of the September 11 attacks.

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Former Washington Wizards forward Pope Jones was a teammate of Jordans during the 2001-02 season in Washington. Jones is now an assistant coach with the Indiana Pacers, and last week, he shared that Michael Jordan told them he was going to show them how to score 20 points in a quarter and then sit down for the rest of the game.

We were playing in one of the first preseason games we were playing [the] Miami [Heat], and we were in the tunnel getting ready to walk out. And again, it was a preseason game, and he [Michael Jordan] said Im going to show you guys how to get 20 points in a quarter and sit down, and at the end of one, he had 18. Then he went ahead and sat down. That was unique, and I think one of the first practices because we know the type of scorer he was, but we all know that Jones told me. I didnt know the kind of playmaker he was until he showed us during practice, he was shooting every time and scoring. Coach Doug Collins said Michael, you cant shoot anymore, and then he looked like he was John Stockton or Magic Johnson with his passing and his vision, which really impressed me. I said something to him, and he said I see everybody I just want to score.

Jordan would end in 2002, due to torn cartilage in his right knee ended Jordans season after only 60 games.

READ NEXT: Charles Barkley Auctioning off Memorabilia to Build Affordable Housing in Alabama

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General Hospital recap: Jordan is Forced to Work For Cyrus to Save TJ – Soaps.com

Franco and Liz go to The Floating Rib. Spinelli and Sam enter, discussing Obrecht being locked up. Franco overhears this and asks for details. They explain Anna arrested her for trying to kill him. He refuses to believe Liesl would do that. Liz encourages him to go and see his friend. Across the room, Sam tells Spinelli he needs to keep his mouth shut about Peter. Hes worried about Maxie, but Sam insists they cant even warn her. She heads over to the bar and talks to Liz, who fills her in about Jason saving Cam. This is all news to Sam.

Nina is shown into the cells to see her aunt. Obrecht quickly realizes her niece may think shes guilty and insists that Peter has framed her for his crimes. This is hard for Nina to believe. Liesl insists that she has changed while August is just a fake. When Obrecht says that Nathan would want her to help, thats the last straw for Nina, who storms out, declaring this is all Liesls own fault. Later, Franco drops by. Obrecht tells him this is all nonsense and insists she would never try to kill him. He reminds her of their past betrayals. Liesl insists she wasnt involved in the demented Drew story. Franco asks for a reason to believe her. She explains that Peter framed her. Hes not sure he can believe her and walks out.

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Willow and Chase go to Charlies and talk about how annoying Nelle is. Harmony wanders in and almost leaves but her daughter asks her to sit down. The women talk about how they are coping. After Harmony gets a text, she rushes off, telling her daughter she really appreciates the second chance. Chase hadnt realized that Willow was so close to her mom again. Shes proud of her mom for turning on Shiloh and doesnt want to waste another chance with her. He hopes shes not disappointed. Julian interrupts and thanks Willow for taking Nelle down a notch. She admits to Chase she threw a drink in her face. Meanwhile, Britt sits at the bar and talks to Julian about Brad. She admires him for all he did for his husband. Jerome guesses she knows he was involved, and she admits Brad told her everything. Julian explains that Brad was blackmailing him and refused to listen to anything he said. They do shots and she points out how much hes alienated his family. She keeps drinking and tells him she feels like letting loose. They head to his office and have sex on the couch.

More: Soap alum voice characters in SCOOB!

At the Quartermaine estate, Michael and Sasha discuss how getting married would help with his custody case. She admits she didnt think she was ready for motherhood, but after her run-in with Nelle, shed be happy just to keep Wiley away from that awful woman. They discuss how lucky they are and how strong they are together. He drops down on a knee and proposes. She agrees and they kiss. He calls Diane over and they announce they are getting married. The lawyer says this is an awful idea. She points out that Sasha doesnt have a great record, and this would look bad in court. The lawyer suggests he marry someone with good credentials or not at all. After she exits, Michael apologizes and wishes things were different. Sasha is disappointed and wonders what to do now.

At home, Jordan gets a text warning her to stay silent about TJ. Curtis asks what it is, but she lies about it. He calms her down as she gets upset talking about her visit to Pentonville to see Cyrus. She asks him to take Stella out so she can have time alone. After she heads to her room, Curtis offers to take Stella out. Shes reluctant but he insists and has even booked her a room at the Metro Court. Once they are gone, Jordan sends a text to say shes alone. Soon, Harmony shows up. Cyrus sent her. Thats bewildering to Jordan. Harmony explains that she will be relaying Cyrus messages and the cop will have to work for the gangster. If she refuses, it will be bad for TJ. She warns that Cyrus reach is a lot further than she knows and hands her a burner phone. Jordan demands daily proof her son is alive.

More: Interview with Emmy nominee Gregory Zarian

Back at The Floating Rib, Stella tells Curtis about her time in Amsterdam. Shes sure hes worried about what his wife is keeping from him. Nina wanders in and joins them. They talk about her aunt getting arrested. She actually thinks Obrecht is guilty.

Curtis goes home and is surprised to see Jordan is still awake. Shes upset and doesnt know where to hit Cyrus. He says they just need to find his weak spot.

On the next General Hospital:

Bad news comes for Sonny.

Jordan gives Sam some false information.

Curtis is startled.

Link:

General Hospital recap: Jordan is Forced to Work For Cyrus to Save TJ - Soaps.com

Understanding SARS-CoV-2 and the drugs that might lessen its power – The Economist

Mar 12th 2020

THE INTERCONNECTEDNESS of the modern world has been a boon for SARS-CoV-2. Without planes, trains and automobiles the virus would never have got this far, this fast. Just a few months ago it took its first steps into a human host somewhere in or around Wuhan, in the Chinese province of Hubei. As of this week it had caused over 120,000 diagnosed cases of covid-19, from Troms to Buenos Aires, Alberta to Auckland, with most infections continuing to go undiagnosed (see article).

But interconnectedness may be its downfall, too. Scientists around the world are focusing their attention on its genome and the 27 proteins that it is known to produce, seeking to deepen their understanding and find ways to stop it in its tracks. The resulting plethora of activity has resulted in the posting of over 300 papers on MedRXiv, a repository for medical-research work that has not yet been formally peer-reviewed and published, since February 1st, and the depositing of hundreds of genome sequences in public databases. (For more coverage of covid-19 see our coronavirus hub.)

The assault on the vaccine is not just taking place in the lab. As of February 28th Chinas Clinical Trial Registry listed 105 trials of drugs and vaccines intended to combat SARS-CoV-2 either already recruiting patients or proposing to do so. As of March 11th its American equivalent, the National Library of Medicine, listed 84. This might seem premature, considering how recently the virus became known to science; is not drug development notoriously slow? But the reasonably well-understood basic biology of the virus makes it possible to work out which existing drugs have some chance of success, and that provides the basis for at least a little hope.

Even if a drug were only able to reduce mortality or sickness by a modest amount, it could make a great difference to the course of the disease. As Wuhan learned, and parts of Italy are now learning, treating the severely ill in numbers for which no hospitals were designed puts an unbearable burden on health systems. As Jeremy Farrar, the director of the Wellcome Trust, which funds research, puts it: If you had a drug which reduced your time in hospital from 20 days to 15 days, thats huge.

Little noticed by doctors, let alone the public, until the outbreak of SARS (severe acute respiratory syndrome) that began in Guangdong in 2002, the coronavirus family was first recognised by science in the 1960s. Its members got their name because, under the early electron microscopes of the period, their shape seemed reminiscent of a monarchs crown. (It is actually, modern methods show, more like that of an old-fashioned naval mine.) There are now more than 40 recognised members of the family, infecting a range of mammals and birds, including blackbirds, bats and cats. Veterinary virologists know them well because of the diseases they cause in pigs, cattle and poultry.

Virologists who concentrate on human disease used to pay less attention. Although two long-established coronaviruses cause between 15% and 30% of the symptoms referred to as the common cold, they did not cause serious diseases in people. Then, in 2002, the virus now known as SARS-CoV jumped from a horseshoe bat to a person (possibly by way of some intermediary). The subsequent outbreak went on to kill almost 800 people around the world.

Some of the studies which followed that outbreak highlighted the fact that related coronaviruses could easily follow SARS-CoV across the species barrier into humans. Unfortunately, this risk did not lead to the development of specific drugs aimed at such viruses. When SARS-CoV-2similarly named because of its very similar genomeduly arrived, there were no dedicated anti-coronavirus drugs around to meet it.

A SARS-CoV-2 virus particle, known technically as a virion, is about 90 nanometres (billionths of a metre) acrossaround a millionth the volume of the sort of cells it infects in the human lung. It contains four different proteins and a strand of RNAa molecule which, like DNA, can store genetic information as a sequence of chemical letters called nucleotides. In this case, that information includes how to make all the other proteins that the virus needs in order to make copies of itself, but which it does not carry along from cell to cell.

The outer proteins sit athwart a membrane provided by the cell in which the virion was created. This membrane, made of lipids, breaks up when it encounters soap and water, which is why hand-washing is such a valuable barrier to infection.

The most prominent protein, the one which gives the virions their crown- or mine-like appearance by standing proud of the membrane, is called spike. Two other proteins, envelope protein and membrane protein, sit in the membrane between these spikes, providing structural integrity. Inside the membrane a fourth protein, nucleocapsid, acts as a scaffold around which the virus wraps the 29,900nucleotides of RNA which make up its genome.

Though they store their genes in DNA, living cells use RNA for a range of other activities, such as taking the instructions written in the cells genome to the machinery which turns those instructions into proteins. Various sorts of virus, though, store their genes on RNA. Viruses like HIV, which causes AIDS, make DNA copies of their RNA genome once they get into a cell. This allows them to get into the nucleus and stay around for years. Coronaviruses take a simpler approach. Their RNA is formatted to look like the messenger RNA which tells cells what proteins to make. As soon as that RNA gets into the cell, flummoxed protein-making machinery starts reading the viral genes and making the proteins they describe.

First contact between a virion and a cell is made by the spike protein. There is a region on this protein that fits hand-in-glove with ACE2, a protein found on the surface of some human cells, particularly those in the respiratory tract.

ACE2 has a role in controlling blood pressure, and preliminary data from a hospital in Wuhan suggest that high blood pressure increases the risks of someone who has contracted the illness dying of it (so do diabetes and heart disease). Whether this has anything to do with the fact that the viruss entry point is linked to blood-pressure regulation remains to be seen.

Once a virion has attached itself to an ACE2 molecule, it bends a second protein on the exterior of the cell to its will. This is TMPRSS2, a protease. Proteases exist to cleave other proteins asunder, and the virus depends on TMPRSS2 obligingly cutting open the spike protein, exposing a stump called a fusion peptide. This lets the virion into the cell, where it is soon able to open up and release its RNA (see diagram).

Coronaviruses have genomes bigger than those seen in any other RNA virusesabout three times longer than HIVs, twice as long as the influenza viruss, and half as long again as the Ebola viruss. At one end are the genes for the four structural proteins and eight genes for small accessory proteins that seem to inhibit the hosts defences (see diagram). Together these account for just a third of the genome. The rest is the province of a complex gene called replicase. Cells have no interest in making RNA copies of RNA molecules, and so they have no machinery for the task that the virus can hijack. This means the virus has to bring the genes with which to make its own. The replicase gene creates two big polyproteins that cut themselves up into 15, or just possibly 16, short non-structural proteins (NSPs). These make up the machinery for copying and proofreading the genomethough some of them may have other roles, too.

Once the cell is making both structural proteins and RNA, it is time to start churning out new virions. Some of the RNA molecules get wrapped up with copies of the nucleocapsid proteins. They are then provided with bits of membrane which are rich in the three outer proteins. The envelope and membrane proteins play a large role in this assembly process, which takes place in a cellular workshop called the Golgi apparatus. A cell may make between 100 and 1,000 virions in this way, according to Stanley Perlman of the University of Iowa. Most of them are capable of taking over a new celleither nearby or in another bodyand starting the process off again.

Not all the RNA that has been created ends up packed into virions; leftovers escape into wider circulation. The coronavirus tests now in use pick up and amplify SARS-CoV-2-specific RNA sequences found in the sputum of infected patients.

Because a viral genome has no room for free riders, it is a fair bet that all of the proteins that SARS-CoV-2 makes when it gets into a cell are of vital importance. That makes each of them a potential target for drug designers. In the grip of a pandemic, though, the emphasis is on the targets that might be hit by drugs already at hand.

The obvious target is the replicase system. Because uninfected cells do not make RNA copies of RNA molecules, drugs which mess that process up can be lethal to the virus while not necessarily interfering with the normal functioning of the body. Similar thinking led to the first generation of anti-HIV drugs, which targeted the process that the virus uses to transcribe its RNA genome into DNAanother thing that healthy cells just do not do.

Like those first HIV drugs, some of the most promising SARS-CoV-2 treatments are molecules known as nucleotide analogues. They look like the letters of which RNA or DNA sequences are made up; but when a virus tries to use them for that purpose they mess things up in various ways.

The nucleotide-analogue drug that has gained the most attention for fighting SARS-CoV-2 is remdesivir. It was originally developed by Gilead Sciences, an American biotechnology firm, for use against Ebola fever. That work got as far as indicating that the drug was safe in humans, but because antibody therapy proved a better way of treating Ebola, remdesivir was put to one side. Laboratory tests, though, showed that it worked against a range of other RNA-based viruses, including SARS-CoV, and the same tests now show that it can block the replication of SARS-CoV-2, too.

There are now various trials of remdesivirs efficacy in covid-19 patients. Gilead is organising two in Asia that will, together, involve 1,000 infected people. They are expected to yield results in mid- to late-April. Other nucleotide analogues are also under investigation. When they screened seven drugs approved for other purposes for evidence of activity against SARS-CoV-2, a group of researchers at the State Key Laboratory of Virology in Wuhan saw some potential in ribavirin, an antiviral drug used in the treatment of, among other things, hepatitis C, that is already on the list of essential medicines promulgated by the World Health Organisation (WHO).

Nucleotide analogues are not the only antiviral drugs. The second generation of anti-HIV drugs were the protease inhibitors which, used along with the original nucleotide analogues, revolutionised the treatment of the disease. They targeted an enzyme with which HIV cuts big proteins into smaller ones, rather as one of SARS-CoV-2s NSPs cuts its big polyproteins into more little NSPs. Though the two viral enzymes do a similar job, they are not remotely relatedHIV and SARS-CoV-2 have about as much in common as a human and a satsuma. Nevertheless, when Kaletra, a mixture of two protease inhibitors, ritonavir and lopinavir, was tried in SARS patients in 2003 it seemed to offer some benefit.

Another drug which was developed to deal with other RNA-based virusesin particular, influenzais Favipiravir (favilavir). It appears to interfere with one of the NSPs involved in making new RNA. But existing drugs that might have an effect on SARS-CoV-2 are not limited to those originally designed as antivirals. Chloroquine, a drug mostly used against malaria, was shown in the 2000s to have some effect on SARS-CoV; in cell-culture studies it both reduces the viruss ability to get into cells and its ability to reproduce once inside them, possibly by altering the acidity of the Golgi apparatus. Camostat mesylate, which is used in cancer treatment, blocks the action of proteases similar to TMPRSS2, the protein in the cell membrane that activates the spike protein.

Not all drugs need to target the virus. Some could work by helping the immune system. Interferons promote a widespread antiviral reaction in infected cells which includes shutting down protein production and switching on RNA-destroying enzymes, both of which stop viral replication. Studies on the original SARS virus suggested that interferons might be a useful tool for stopping its progress, probably best used in conjunction with other drugs

Conversely, parts of the immune system are too active in covid-19. The virus kills not by destroying cells until none are left, but by overstimulating the immune systems inflammatory response. Part of that response is mediated by a molecule called interleukin-6one of a number of immune-system modulators that biotechnology has targeted because of their roles in autoimmune disease.

Actemra (tocilizumab) is an antibody that targets the interleukin-6 receptors on cell surfaces, gumming them up so that the interleukin-6 can no longer get to them. It was developed for use in rheumatoid arthritis. China has just approved it for use against covid-19. There are anecdotal reports of it being associated with clinical improvements in Italy.

While many trials are under way in China, the decline in the case rate there means that setting up new trials is now difficult. In Italy, where the epidemic is raging, organising trials is a luxury the health system cannot afford. So scientists are dashing to set up protocols for further clinical trials in countries expecting a rush of new cases. Dr Farrar said on March 9th that Britain must have its trials programme agreed within the week.

International trials are also a high priority. Soumya Swaminathan, chief scientist at the WHO, says that it is trying to finalise a master protocol for trials to which many countries could contribute. By pooling patients from around the world, using standardised criteria such as whom to include and how to measure outcomes, it should be possible to create trials of thousands of patients. Working on such a large scale makes it possible to pick up small, but still significant, benefits. Some treatments, for example, might help younger patients but not older ones; since younger patients are less common, such an effect could easily be missed in a small trial.

The caseload of the pandemic is hard to predict, and it might be that even a useful drug is not suitable in all cases. But there are already concerns that, should one of the promising drugs prove to be useful, supplies will not be adequate. To address these, the WHO has had discussions with manufacturers about whether they would be able to produce drugs in large enough quantities. Generic drug makers have assured the organisation that they can scale up to millions of doses of ritonavir and lopinavir while still supplying the HIV-positive patients who rely on the drugs. Gilead, meanwhile, has enough remdesivir to support clinical trials and, thus far, compassionate use. The firm says it is working to make more available as rapidly as possible, even in the absence of evidence that it works safely.

In the lab, SARS-CoV-2 will continue being dissected and mulled over. Details of its tricksiness will be puzzled out, and the best bits of proteins to turn into vaccines argued over. But that is all for tomorrow. For today doctors can only hope that a combination of new understanding and not-so-new drugs will do some good.

Dig deeper:

This article appeared in the Briefing section of the print edition under the headline "Anatomy of a killer"

See the rest here:

Understanding SARS-CoV-2 and the drugs that might lessen its power - The Economist

Marine medicine: Understanding and treating infection types – National Fisherman

Many fishermen come to believe that they have a natural immunity to infections, but the reality is quite the contrary. Infections have shut down fishing operations across the world, which is why its essential to both understand infection types that cause symptoms as well as what sort of preventative measures can be taken to avoid them entirely. preventions in todays world.

As a baseline for this topic, the definition of an infection is the invasion of an organisms body tissue (man or beast) by disease-causing agents. An agent can be bacteria, viruses, fungus and parasites. Infections can be transmitted in a variety of ways.

Exactly how an infection can spread as well as its effect on the human body depends on the type of infective agent. Some infectious diseases can be passed from one person to another easily while others are harder to transmit. The flu, a cold, measles or a sore throat may be transmitted by a kiss or a simple touch or cough from one person to another. Infectious diseases such as AIDS, herpes and hepatitis are only passed by a closer contact called bloodborne transmission as blood to blood or sexual intercourse.

Some examples of how infections are transmissible, communicable of contagious are:

There are many different root causes of these infections, all of which need to be fully understood in order to determine the best approach for prevention and treatment.

Bacteria Infection

Most of the Earths biomass is made of bacteria, which are single-celled micro-organisms. Bacteria can live in almost any kind of environment which ranges from extreme heat to intense cold. Some can even survive in radioactive waste. Bacteria are also highly adaptable. That can cause problems for people because it often results in resistance to antibiotics.

There are trillions of strains of bacteria and a few of these may cause diseases in humans. Some bacteria are beneficial to human digestion and airways. However, there are also plenty of good bacteria like the digestive bacteria contained in our stomachs.

Some examples of bacteria diseases are:

Bacterial infections can be treated with antibiotics but some strains become resistant and can survive treatment. Antibiotics resistant bacterial infections and or diseases have been an ever-increasing which has become a major a concern to infectious diseases specialists and the CDC (Center for Disease Control).

Viral infections

Viral infections are as numerous and as deadly as bacterial diseases. Viral infections can range from the common cold to Ebola. Unlike bacteria, viruses are made up of only a genetic code that is encapsulated in a shell made up of protein and fat.

Viruses invade a host and attach to the hosts cell. By this process of attachment and release of genetics (commanding seed matter), the virus rapidly replicates and kills the host cells only to go on to infect new cells and repeats the cycle. Since the virus is only genetic material, it may remain dormant and reactivate when conditions demand so.

Some examples of viral infections are:

Antiviral medications can help in some cases as they can either prevent the virus from reproducing or boost the bodys immune system response. Antibiotics are not effective against viruses but most treatments are directed to relieve symptoms while the immune system combats the virus without assistance from drugs and treatments.

Fungal infections

A fungus is a many-celled parasite that can reproduce by spreading spores. Many fungal infections will appear on the topical skin as a persistent rash. Inhaled fungal spores can cause thrush and candidiasis.

Examples of fungal infections are:

Since commercial fishermen work in such harsh environments, the demands of the bodys protective immune system are much greater. A healthy active lifestyle can help keep the immune system strong and able to defend the body against different kinds of infections. Fishermen can stop the spread of communicable diseases with some simple common sense procedures that can be followed on their vessels and onshore.

There is no single way to prevent all infectious diseases. However, the following tips can reduce the risk of transmission:

Given how much they are handling gear and fish, the majority of commercial fishermens on-the-job infections are infections of the fingers and hands. Thats why its especially important to understand what it means to understand these types of infections.

Treating and preventing infections of the fingers and hands

Fish and fish products are often contaminated with infectious bacteria, which explains why fishermen are so prone to infections via the involuntary penetration into soft tissue by fish spines and bones. Bacteria can be easily carried into these open wounds by fish slime, fish intestinal parts and contaminated vessel components. Additionally, the handling of ropes, cables and moving metal parts in the unpredictable environment of the sea adds to the likelihood of bloody injuries that are centered on the hands.

Prevention is always better than treatment. All finger and hand infections are very painful and disabling. Some infections can cause permanent disability, possibly ending a fishermans career. Infections in the hands should always be treated aggressively within the following guidelines:

Knives and fishhooks

Injuries caused by a fishermans working tools such as knives and fishhooks should be treated aggressively and immediately. These instruments can directly inject harmful bacteria deep in the soft tissue.

In order to remove a fishhook with the minimum tissue damage, follow this simple procedure:

The ability to give and receive proper medical attention while at sea is extremely limited. Thats why your medical skills and the supplies you have on hand can make all the difference. Preventing injuries is always the most cost-effective action plan, but that underscores why its essential to get proper training, be prepared, but most importantly, always think safety first.

For additional information concerning the best medical kit for your vessel visit marinemedical.com or email your request to info@marinemedical.com.You can also reach us by calling 800-272-3008.

Continued here:

Marine medicine: Understanding and treating infection types - National Fisherman

Coronavirus vaccines and treatment: Everything you need to know – CNET

Everything you need to know about COVID-19 vaccines.

COVID-19, the potentially fatal respiratory illness first detected in December 2019, has spread across the globe,forcing the cancellation of major events, postponing sports seasons and sending many into self-imposed quarantine. As health authorities and governments attempt to slow the spread, researchers are focusing their attention on the coronavirus that causes the disease: SARS-CoV-2.

Since it was first discovered as the causative agent of the new disease, scientists have been racing to get a better understanding of the virus' genetic makeup, how it infects cells and how to effectively treat it. Currently there's no cure and medical specialists can only treat the symptoms of the disease. However, the long-term strategy to combat COVID-19, which has spread to every continent on Earth besides Antarctica, will be to develop a vaccine.

Developing new vaccines takes time and they must be rigorously tested and confirmed safe via clinical trials before they can be routinely used in humans. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases in the US, has commonly stated a vaccine is at least a year to 18 months away. Experts agree there's a ways to go yet.

Vaccines are incredibly important in the fight against disease. We've been able to keep a handful of viral diseases at bay for decades because of vaccine development. Even so, there exists confusion and unease about their usefulness. This guide explains what vaccines are, why they are so important and how scientists will use them in the fight against the coronavirus. As more candidates appear and are tested, we'll add them to this list, so bookmark this page and check back for the latest updates.

You can jump to any segment by clicking the links below:

A vaccine is a type of treatment aimed at stimulating the body's immune system to fight against infectious pathogens, like bacteria and viruses. They are,according to the World Health Organization, "one of the most effective ways to prevent diseases."

The human body is particularly resilient to disease, having evolved a natural defense system against nasty disease-causing microorganisms like bacteria and viruses. The defense system -- our immune system -- is composed of different types of white blood cells that can detect and destroy foreign invaders. Some gobble up bacteria, some produce antibodies which can tell the body what to destroy and take out the germs and other cells memorize what the invaders look like, so the body can respond quickly if they invade again.

Vaccines are a really clever fake-out. They make the body think it's infected so it stimulates this immune response. For instance, the measles vaccine tricks the body into thinking it has measles. When you are vaccinated for measles, your body generates a record of the measles virus. If you come into contact with it in the future, the body's immune system is primed and ready to beat it back before you can get sick.

The very first vaccine was developed by a scientist named Edward Jenner in the late 18th century. In a famous experiment, Jenner scraped pus from a milkmaid with cowpox -- a type of virus that causes disease mostly in cows and is very similar to the smallpox virus -- and introduced the pus into a young boy. The young boy became a little ill and had a mild case of cowpox. Later, Jenner inoculated the boy with smallpox, but he didn't get sick. Jenner's first injection of cowpox pus trained the boy's body to recognize the cowpox virus and, because its so similar to smallpox, the young man was able to fight it off and not get sick.

Vaccines have come an incredibly long way since 1796 though. Scientists certainly don't inject pus from patients into other patients and vaccines must abide by strict safety regulations, multiple rounds of clinical testing and strong governmental guidelines before they can be adopted for widespread use.

Vaccines contain a handful of different ingredients depending on their type and how they aim to generate an immune response. However, there's some commonality between them all.

The most important ingredient is the antigen. This is the part of the vaccine the body can recognize as foreign. Depending on the type of vaccine, an antigen could be molecules from viruses like a strand of DNA or a protein. It could instead be weakened versions of live viruses. For instance, the measles vaccine contains a weakened version of the measles virus. When a patient receives the measles vaccine, their immune system recognizes a protein present on the measles virus and learns to fight it off.

A second important ingredient is the adjuvant. An adjuvant works to amplify the immune response to an antigen. Whether a vaccine contains an adjuvant depends on the type of vaccine it is.

Some vaccines used to be stored in vials that could be used multiple times and, as such, contained preservatives that ensured they would be able to sit on a shelf without growing other nasty bacteria inside them. One such preservative is thimerosal which has garnered a lot of attention in recent times because it contains trace amounts of the easily-cleared ethylmercury. Its inclusion in vaccines has not been shown to cause harm, according to the CDC. In places like Australia, single-use vials are now common and thus preservatives such as thimerosal are no longer necessary in most vaccines.

In developing a vaccine for SARS-CoV-2, scientists need to find a viable antigen that will stimulate the body's immune system into defending against infection.

The pathogen at the center of the outbreak, SARS-CoV-2, belongs to the family of viruses known ascoronaviruses. This family is so named because, under a microscope, they appear with crown-like projections on their surface.

In developing a vaccine that targets SARS-CoV-2, scientists are looking at these projections intensely. The projections enable the virus to enter human cells where it can replicate and make copies of itself. Known as "spike proteins" or "S" proteins, researchers have been able to map the projections in 3Dand research suggests they could be a viable antigen in any coronavirus vaccine.

That's because the S protein is prevalent in coronaviruses we've battled in the past -- including the one that caused the SARS outbreak in China in 2002-2003. This has given researchers a head start on building vaccines against part of the S protein and, using animal models, have demonstrated they can generate an immune response.

There are many other companies across the world working on a SARS-CoV-2 vaccine, developing different ways to stimulate the immune system. Some of the most talked about approaches are those using a relatively novel type of vaccine known as a "nucleic acid vaccine." These vaccines are essentially programmable, containing a small piece of genetic code to act as the antigen.

Biotech companies like Moderna have been able to generate new vaccine designs against SARS-CoV-2 rapidly by taking a piece of the genetic code for the S protein and fusing it with fatty nanoparticles that can be injected into the body. Imperial College London is designing a similar vaccine using coronavirus RNA -- its genetic code. Pennsylvania biotech company Inovio is generating strands of DNA it hopes will stimulate an immune response. Although these kinds of vaccines can be created quickly, none have been brought to market yet.

Johnson & Johnson and French pharmaceutical giant Sanofi are both working with the US Biomedical Advanced Research and Development Authority to develop vaccines of their own. Sanofi's plan is to mix coronavirus DNA with genetic material from a harmless virus, whereas Johnson & Johnson will attempt to deactivate SARS-CoV-2, essentially switching off its ability to cause illness while ensuring it still stimulates the immune system.

Some research organizations, such as Boston Children's Hospital, are examining different kinds of adjuvants that will help amplify the immune response. This approach, according to the Harvard Gazette, will be targeted more towards the elderly, who don't respond as effectively when vaccinated. It's hoped that by studying adjuvants to boost a vaccine, the elderly will be able to be vaccinated with a mix of ingredients that can supercharge their immunity.

Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases in the US, posits that a vaccine is at least a year and a half away, even though we're likely to see human trials start within the next month or two. This, according to a 60 Minutes interview with Fauci in March, is a fast turnaround.

"The good news is we did it more quickly than we've ever done it," Fauci told 60 Minutes in March. "The sobering news is that it's not ready for primetime, for what we're going through now."

Why does vaccine production take so long? There's a ton of steps involved and a lot of regulatory hurdles to jump through.

"For any medicine to be sold it needs to go through the standard process of clinical trials including phase 1 [to] 3 trials," says Bruce Thompson, dean of health at Swinburne University in Australia. "We need to ensure that the medicine is safe, will not do harm, and know how effective it is."

Scientists can't assume their vaccine design will just work -- they have to test, test and test again. They have to recruit thousands of people to ensure the safety of a vaccine and how useful it will be. The process can be broken down into six phases:

Traditionally then, it could take a decade or more for a new vaccine to go from design to approval. In addition, once the regulatory processes have concluded a vaccine is safe, the drug companies have to send production into overdrive, so they can manufacture enough of the vaccine to increase immunity in the wider population.

With SARS-CoV-2, the process is being expedited in some instances. As STATnews reports, the vaccine in development by Moderna has moved from design straight into Phase I clinical trials of it mRNA vaccine, skipping tests in animal models. Those tests will take place at Seattle's Kaiser Permanente Washington Health Instituteand patients are now being enrolled.

Until that time though, health workers, doctors and medical specialists must rely on current treatment options.

The best way to prevent illness is avoiding exposure. Those tips are below.

First: Antibiotics, medicine designed to fight bacteria, won't work on SARS-CoV-2, a virus. If you're infected, you will be asked to self-isolate, to prevent further spread of the disease, for 14 days. If symptoms escalate and you experience a shortness of breath, high fever and lethargy, you should seek medical care.

Treating cases of COVID-19 in the hospital is based on managing patient symptoms in the most appropriate way. For patients with severe disease adversely affecting the lungs, doctors place a tube into a patient's airway so that they can be connected to ventilators -- machines which help control breathing.

There are no specific treatments for COVID-19 as yet, though a number are in the works including experimental antivirals, which can attack the virus, and existing drugs targeted at other viruses like HIV which have shown some promise in treating COVID-19.

Remdesivir

Remdesivir, an experimental antiviral made by biotech firm Gilead Sciences, has garnered a lion's share of the limelight. The drug has been used in the US, China and Italy, but only on a "compassionate basis" -- essentially, this drug has not received approval but can be used outside of a clinical trial on critically ill patients. Remdesivir is not specifically designed to destroy SARS-CoV-2. Instead, it works by knocking out a specific piece of machinery in the virus, known as "RNA polymerase," which many viruses use to replicate. It has been shown as effective in human cells and mouse models in the past.

It's effectiveness is still being debated and much more rigorous study will be needed before this becomes a general treatment for SARS-CoV-2, if it does at all.

Other treatment options

A HIV medicine, Kaletra/Aluvia, has been used in China to treat COVID-19. According to a release by AbbVie, an Illinois-based pharmaceutical company, the treatment was provided as an experimental option for Chinese patients during "the early days" of fighting the virus. The company suggests it is collaborating with global health authorities including the CDC and WHO.

A drug that has been used to treat malaria for around 70 years, chloroquine, has been floated as a potential candidate. It appears to be able to block viruses from binding to human cells and getting inside them to replicate. It also stimulates the immune system. A letter to the editor in journal Nature on Feb. 4 showed chloroquine was effective in combating SARS-CoV-2. Another Chinese study emanating from Guangdong reports chloroquine improved patient outcomesand "might improve the success rate of treatment" and "shorten hospital stay."

It is not a good idea to rely on a vaccine to stop the spread of coronavirus because they are many months away. The best way to stop the spread, right now, is to continue practicing good personal hygiene and to limit interactions with others. "The best thing to do is the simple things like hand washing and hand sanitizing," notes Thompson.

This outbreak is unprecedented and changing behaviors is absolutely critical to stopping the spread.

There are a huge number of resources available from the WHO on protecting yourself against infection. It's clear the virus can spread from person-to-person and transmission in communities has occurred across the world. Protection boils down to a few key things:

For much more information, you can head to CNET's guide

Read more:

Coronavirus vaccines and treatment: Everything you need to know - CNET

On the front lines of developing a test for the coronavirus – Jacksonville Journal-Courier

David Pride, University of California San Diego

(The Conversation is an independent and nonprofit source of news, analysis and commentary from academic experts.)

David Pride, University of California San Diego

(THE CONVERSATION) That escalated quickly! is a common trope used in popular culture to describe when a situation gets out of hand before youve even had a chance to think about it. We dont often use this trope in medicine, but I can think of nothing better to describe what has been going on in the U.S. with the coronavirus outbreak.

I am a physician scientist who practices infectious disease medicine and runs a research laboratory that specializes in viruses. I spend much of my time directing a clinical microbiology laboratory for a large academic medical center. If youve ever had a doctor tell you that they are going to test you for a virus, its teams like mine that develop and run that test.

When I first heard about the coronavirus outbreak in China, I had no idea I would soon be on the front lines of dealing with this outbreak.

Why testing is at the heart of the problem

Let me start by describing exactly what this virus is. Its a novel virus from the coronavirus family and is spread by respiratory droplets (like when you sneeze) and contact with contaminated surfaces. The common cold is usually caused by rhinoviruses, but there are four coronaviruses that also cause colds.

The SARS outbreak of 2003 resulted in 774 deaths and the MERS outbreak of 2012 resulted in 858 deaths; both were caused by novel coronaviruses. The ease of spread of this new virus called SARS-CoV-2 has led to its rapid emergence across the globe, with more than 5,000 deaths and counting. Although there are drugs in development and testing phases, there are no drugs currently available that are proven effective against severe coronavirus illnesses.

For the most part, public health officials dont know who in the U.S. has it because there isnt a method to test most of the population for it. If you dont know who has a disease, its impossible to predict its spread, how many people will get it, or how many people may die from it. Testing in the U.S. must be expanded, which a number of companies are working on, to reveal the scope of the problem.

How the US lagged behind

Earlier this year, the Centers for Disease Control and Prevention developed a rapid test for SARS-CoV-2. This test is designed to amplify and detect the genetic material in the virus its RNA (ribonucleic acid) from your body. It targets certain conserved RNA sequences in the virus that are different from those found in other coronaviruses. The problem is that for a population of 331 million, a single testing center wasnt nearly enough. The CDC enabled state public health labs to use their test, but this still hasnt been enough to meet population needs.

The testing deficiency leaves much of the U.S. population out in the cold. Its now up to companies, hospitals and academic centers to pick up the slack. Part of the delay was due to what happened during the Zika virus outbreak of 2015, when laboratories that developed their own tests were halted by the FDA because they did not have approval.

Testing development really picked up Feb. 29 after the FDA relented and released guidance for developing tests in individual laboratories, and a free-for-all ensued. We laboratory directors were on the spot to develop tests, and most were unprepared to say the least. Test development typically takes months.

Labs use what is called a reverse-transcription polymerase chain reaction, or RT-PCR, to test a sample taken with a swab from the back of someones throat and/or nose. The tests work by converting the virus RNA to DNA and then replicating it millions of times in order to amplify its presence and then detect its genetic sequence. If it is detected, a patient is infected.

Even with the FDA guidance, we had to decide what RNA sequences in the virus to target and how quickly we could get reliable testing materials. We could only obtain materials for RNA amplification and detection from the CDC or private industry, who were all being bombarded with our requests simultaneously. We laboratory directors were suddenly competing with one another for limited resources to develop these tests.

What went wrong?

If you compare our ability to ramp up testing to that observed in Chinaand South Korea, the U.S. response was not up to par. Both countries allowed companies to develop and distribute tests from an early stage, permitting large portions of their populations to be tested.

Part of the problem in the U.S. is the lack of centralized facilities across the country that all have the same equipment to run complex tests. Just in the state of California alone where I live, there are hundreds of hospitals, most with significant differences in their equipment and testing capabilities. When the CDC made their test available, my first thought was, We dont even have the equipment to run this test. Most hospitals in my state and across the country faced this exact same dilemma: a lack of proper equipment and difficulty obtaining adequate testing materials.

Also, problems with CDC-manufactured testing kits arose immediately and caused testing failures when they first released them in February. These failure stories motivated many of us to either develop tests based on our own analysis of COVID-19, or to partner with industry in the development of their tests. At my institution, weve been working with industry partners and accelerating the development of their tests for our patient populations.

Why its not the end of the world

Theres a lot of negatives to find in the response to the coronavirus outbreak, but the flaws in the response represent learning opportunities. Highly infectious viruses in a connected world wont stay contained for long. Our assumption should have been that it would make it to the U.S. from the onset.

The next time theres an outbreak, we laboratory directors wont be waiting for the government to give us the green light to develop diagnostic tests. Well do it on our own and press the FDA to allow us to use it. The hard work to ramp up testing in the U.S. is the most significant effort in which I have ever taken part. If you could see the efforts of companies, academic centers, and hospitals right now in the U.S., youd walk away with optimism that were up to the task.

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This article is republished from The Conversation under a Creative Commons license. Read the original article here: https://theconversation.com/on-the-front-lines-of-developing-a-test-for-the-coronavirus-133124.

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On the front lines of developing a test for the coronavirus - Jacksonville Journal-Courier

Researchers Predict Potential Spread And Seasonality For COVID-19 Based On Climate Where Virus Appears To Thrive – Herald-Mail Media

BALTIMORE, Md., March 16, 2020 /PRNewswire/ --Newswise -- Researchers at the University of Maryland School of Medicine's Institute of Human Virology (IHV), which is part of the Global Virus Network (GVN), predict that COVID-19 will follow a seasonal pattern similar to other respiratory viruses like seasonal flu. They base this on weather modeling data in countries where the virus has taken hold and spread within the community.

In a new paper published on the open-data site SSRN, the researchers found that all cities experiencing significant outbreaks of COVID-19 have very similar winter climates with an average temperature of 41 to 52 degrees Fahrenheit, an average humidity level of 47 to 79 percent with a narrow east-west distribution along the same 30-50 N" latitude. This includes Wuhan, China, South Korea, Japan, Iran, Northern Italy, Seattle, and Northern California. It could also spell increasing trouble for the Mid-Atlantic States and -- as temperatures rise -- New England.

"Based on what we have documented so far, it appears that the virus has a harder time spreading between people in warmer, tropical climates," said study leader Mohammad Sajadi, MD, Associate Professor of Medicine at the Insitute of Human Virology at the UMSOM and a member of GVN. "That suggests once average temperatures rise above 54 degrees Fahrenheit (12 degrees Celsius) and higher, the virus may be harder to transmit, but this is still a hypothesis that requires more data."

The team based its predictions on weather data from the previous few months as well as typical patterns from last year to hypothesize on community spread within the next few weeks. "Using 2019 temperature data for March and April, risk of community spread could be predicted to occur in areas just north of the current areas at risk," said study co-author Augustin Vintzileos, PhD, Assistant Research Scientist in the Earth System Science Interdisciplinary Center at the University of Maryland, College Park. He plans to do further modeling of current weather data to help provide more certainty to the predictions.

Researchers from Shiraz University of Medical Sciences in Shiraz, Iran, and Shaheed Beheshti University of Medical Sciences in Tehran, Iran also participated in this study.

"I think what is important is this is a testable hypotheses," said study co-author Anthony Amoroso, MD, UMSOM Associate Professor of Medicine and Associate Chief of Infectious Diseases who is also Chief of Clinical Care Programs for IHV. "And if it holds true, could be very helpful for health system preparation, surveillance and containment efforts."

In areas where the virus has already spread within the community, like Wuhan, Milan, and Tokyo, temperatures did not dip below the freezing mark, the researchers pointed out. They also based their predictions on a study of the novel coronavirus in the laboratory, which found that a temperature of 39 degrees Fahrenheit and humidity level of 20 to 80 percent is most conducive to the virus's survival.

"Through this extensive research, it has been determined that weather modeling could potentially explain the spread of COVID-19, making it possible to predict the regions that are most likely to be at higher risk of significant community spread in the near future," said Robert C. Gallo Co-founder & Director, Institute of Human Virology at the University of Maryland School of Medicine and Co-Founder and Chairman of the International Scientific Leadership Board of the GVN. Dr. Gallo is also The Homer & Martha Gudelsky Distinguished Professor in Medicine and Director, Institute of Human Virology at the University of Maryland School of Medicine, a GVN Center of Excellence. "In addition to climate variables, there are multiple factors to be considered when dealing with a pandemic, such as human population densities, human factors, viral genetic evolution and pathogenesis. This work illustrates how collaborative research can contribute to understanding, mitigating and preventing infectious threats."

Dr. Gallo is a co-founder of the Global Virus Network, which is a consortium of leading virologists spanning 53 Centers of Excellence and nine Affiliates in 32 countries worldwide, working collaboratively to train the next generation, advance knowledge about how to identify and diagnose pandemic viruses, mitigate and control how such viruses spread and make us sick, as well as develop drugs, vaccines and treatments to combat them. The Network has been meeting regularly to discuss the COVID-19 pandemic sharing their expertise in all viral areas and their research findings.

"This study raises some provocative theories that, if correct, could be useful in helping to direct public health strategies," said UMSOM Dean E. Albert Reece, MD, PhD, MBA, who is also University Executive Vice President for Medical Affairs and the John Z. and Akiko K. Bowers Distinguished Professor. "Perhaps we should be conducting heightened surveillance and expending more resources into areas that currently have the climate that is conducive to community virus spread."

About the Global Virus Network (GVN)

The Global Virus Network (GVN) is essential and critical in the preparedness, defense and first research response to emerging, exiting and unidentified viruses that pose a clear and present threat to public health, working in close coordination with established national and international institutions. It is a coalition comprised of eminent human and animal virologists from 53 Centers of Excellence and nine Affiliates in 32 countries worldwide, working collaboratively to train the next generation, advance knowledge about how to identify and diagnose pandemic viruses, mitigate and control how such viruses spread and make us sick, as well as develop drugs, vaccines and treatments to combat them. No single institution in the world has expertise in all viral areas other than the GVN, which brings together the finest medical virologists to leverage their individual expertise and coalesce global teams of specialists on the scientific challenges, issues and problems posed by pandemic viruses. The GVN is a non-profit 501(c)(3) organization. For more information, please visit http://www.gvn.org. Follow us on Twitter @GlobalVirusNews

About the Institute of Human Virology

Formed in 1996 as a partnership between the State of Maryland, the City of Baltimore, the University System of Maryland and the University of Maryland Medical System, IHV is an institute of the University of Maryland School of Medicine and is home to some of the most globally-recognized and world-renowned experts in all of virology. The IHV combines the disciplines of basic research, epidemiology and clinical research in a concerted effort to speed the discovery of diagnostics and therapeutics for a wide variety of chronic and deadly viral and immune disorders - most notably, HIV the virus that causes AIDS. For more information, http://www.ihv.org and follow us on Twitter @IHVmaryland.

About the University of Maryland School of Medicine

Now in its third century, the University of Maryland School of Medicine was chartered in 1807 as the first public medical school in the United States. It continues today as one of the fastest growing, top-tier biomedical research enterprises in the world -- with 45 academic departments, centers, institutes, and programs; and a faculty of more than 3,000 physicians, scientists, and allied health professionals, including members of the National Academy of Medicine and the National Academy of Sciences, and a distinguished two-time winner of the Albert E. Lasker Award in Medical Research. With an operating budget of more than $1.2 billion, the School of Medicine works closely in partnership with the University of Maryland Medical Center and Medical System to provide research-intensive, academic and clinically based care for nearly 2 million patients each year. The School of Medicine has more than $540 million in extramural funding, with most of its academic departments highly ranked among all medical schools in the nation in research funding. As one of the seven professional schools that make up the University of Maryland, Baltimore campus, the School of Medicine has a total population of nearly 9,000 faculty and staff, including 2,500 student trainees, residents, and fellows. The combined School of Medicine and Medical System ("University of Maryland Medicine") has an annual budget of nearly $6 billion and an economic impact more than $15 billion on the state and local community. The School of Medicine faculty, which ranks as the 8th highest among public medical schools in research productivity, is an innovator in translational medicine, with 600 active patents and 24 start-up companies. The School of Medicine works locally, nationally, and globally, with research and treatment facilities in 36 countries around the world. Visit medschool.umaryland.edu

This news release was issued on behalf of Newswise(TM). For more information, visit http://www.newswise.com.

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Researchers Predict Potential Spread And Seasonality For COVID-19 Based On Climate Where Virus Appears To Thrive - Herald-Mail Media

Rapid genetic testing becomes available to Calgary medical community – CTV News

CALGARY -- When Madden Ellis Garraway was just under two-years-old, he became very sick.

His skin was so dry it bled and he couldnt hold down food, causing his weight dropped to within ounces of his birth weight of seven pounds, six ounces.

Doctors struggled to figure out what was wrong.

We had a large list of things that we were thinking of, and our immunology team and my colleagues who are working with Madden were having trouble arriving at the right one," said Dr. Francois Bernier, head of the Department of Medical Genetics and a professor in the Department of Paediatrics at the University of Calgary's Cumming School of Medicine.

"In fact, we made some attempts to arrive at a diagnosis but we're still unsure. It took a while.

Doctors often struggle with diagnosing unusual health issues, especially those that may require genetic testing.

They often must rely on genome sequencing tests to determine the root cause of a disease and until now, large-scale genome sequencing tests were often sent to labs in the United States for analysis.

Bernier calls it "the diagnostic odyssey," a long, difficult, journey for families waiting while cliniciansfigure out what is causing the underlying health issues.

Madden Garraway in hospital at the age of two. (Photo courtesy the Garraway family)

Maddens family can attest to that.

It was months of waiting, wondering and worrying before Madden's blood was sent to a U.S. lab for genome analysis, where it was learned he suffered from a rare genetic condition called immune dysregulation polyendocrinopathy enteropathy X-linked (IPEX) syndrome.

IPEX is a rare genetic disorder that can be life threatening.

"If we could have learned about that instantly, or within the several weeks that we can do now, that will save a lot of time," said Maddens father, Patrick Garraway.

"We could have got on with his bone marrow transplant sooner."

Madden received a bone marrow transplant from his sister. Now five-years-old, the playful youngster has made a full recovery and no longer requires medication.

"There are so many families waiting for answers to serious medical conditions," said Bernier.

"Access to gene sequencing early in the medical journey can pinpoint the best treatment approaches and therapies to target the illness."

Madden Garraway today at the age of five. (Photo courtesy the Garraway family)

A new partnership struck between the University of Calgary, University of Alberta, and Alberta Precision Laboratorieswill help families and medical professionalsanswer to those diagnostic puzzles sooner.

The partnership is funded by Genome Canada, the Alberta Childrens Hospital Foundation, and other partners. Four other centres in Canada are also undertaking similar programs through Genome Canadas funding, one in B.C., two in Ontario and one in Quebec.

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Rapid genetic testing becomes available to Calgary medical community - CTV News

Race Is Real, But It’s Not Genetic – SAPIENS

Please note that this article includes an image of human remains.

A friend of mine with Central American, Southern European, and West African ancestry is lactose intolerant. Drinking milk products upsets her stomach, and so she avoids them. About a decade ago, because of her low dairy intake, she feared that she might not be getting enough calcium, so she asked her doctor for a bone density test. He responded that she didnt need one because blacks do not get osteoporosis.

My friend is not alone. The view that black people dont need a bone density test is a longstanding and common myth. A 2006 study in North Carolina found that out of 531 African American and Euro-American women screened for bone mineral density, only 15 percent were African American womendespite the fact that African American women made up almost half of that clinical population. A health fair in Albany, New York, in 2000, turned into a ruckus when black women were refused free osteoporosis screening. The situation hasnt changed much in more recent years.

Meanwhile, FRAX, a widely used calculator that estimates ones risk of osteoporotic fractures, is based on bone density combined with age, sex, and, yes, race. Race, even though it is never defined or demarcated, is baked into the fracture risk algorithms.

Lets break down the problem.

First, presumably based on appearances, doctors placed my friend and others into a socially defined race box called black, which is a tenuous way to classify anyone.

Race is a highly flexible way in which societies lump people into groups based on appearance that is assumed to be indicative of deeper biological or cultural connections. As a cultural category, the definitions and descriptions of races vary. Color lines based on skin tone can shift, which makes sense, but the categories are problematic for making any sort of scientific pronouncements.

Second, these medical professionals assumed that there was a firm genetic basis behind this racial classification, which there isnt.

Third, they assumed that this purported racially defined genetic difference would protect these women from osteoporosis and fractures.

The view that black people dont need a bone density test is a longstanding and common myth.

Some studies suggest that African American womenmeaning women whose ancestry ties back to Africamay indeed reach greater bone density than other women, which could be protective against osteoporosis. But that does not mean being blackthat is, possessing an outward appearance that is socially defined as blackprevents someone from getting osteoporosis or bone fractures. Indeed, this same research also reports that African American women are more likely to die after a hip fracture. The link between osteoporosis risk and certain racial populations may be due to lived differences such as nutrition and activity levels, both of which affect bone density.

But more important: Geographic ancestry is not the same thing as race. African ancestry, for instance, does not tidily map onto being black (or vice versa). In fact, a 2016 study found wide variation in osteoporosis risk among women living in different regions within Africa. Their genetic risks have nothing to do with their socially defined race.

When medical professionals or researchers look for a geneticcorrelateto race, they are falling into a trap: They assume thatgeographic ancestry, which does indeed matter to genetics, can be conflated with race, which does not. Sure, different human populations living in distinct places may statistically have different genetic traitssuch as sickle cell trait (discussed below)but such variation is about local populations (people in a specific region), not race.

Like a fish in water, weve all been engulfed by the smog of thinking that race is biologically real. Thus, it is easy to incorrectly conclude that racial differences in health, wealth, and all manner of other outcomes are the inescapable result of genetic differences.

The reality is that socially defined racial groups in the U.S. and most everywhere else do differ in outcomes. But thats not due to genes. Rather, it is due to systemic differences in lived experience and institutional racism.

Communities of color in the United States, for example, often have reduced access to medical care, well-balanced diets, and healthy environments. They are often treated more harshly in their interactions with law enforcement and the legal system. Studies show that they experience greater social stress, including endemic racism, that adversely affects all aspects of health. For example, babies born to African American women are more than twice as likely to die in their first year than babies born to non-Hispanic Euro-American women.

Systemic racism leads to different health outcomes for various populations. The infant mortality rate, for example, for African American infants is double that for European Americans. Kelly Lacy/Pexels

As a professor of biological anthropology, I teach and advise college undergraduates. While my students are aware of inequalities in the life experiences of different socially delineated racial groups, most of them also think that biological races are real things. Indeed, more than half of Americans still believe that their racial identity is determined by information contained in their DNA.

For the longest time, Europeans thought that the sun revolved around the Earth. Their culturally attuned eyes saw this as obvious and unquestionably true. Just as astronomers now know thats not true, nearly all population geneticists know that dividing people into races neither explains nor describes human genetic variation.

Yet this idea of race-as-genetics will not die. For decades, it has been exposed to the sunlight of facts, but, like a vampire, it continues to suck bloodnot only surviving but causing harm in how it can twist science to support racist ideologies. With apologies for the grisly metaphor, it is time to put a wooden stake through the heart of race-as-genetics. Doing so will make for better science and a fairer society.

In 1619, the first people from Africa arrived in Virginia and became integrated into society. Only after African and European bond laborers unified in various rebellions did colony leaders recognize the need to separate laborers. Race divided indentured Irish and other Europeans from enslaved Africans, and reduced opposition by those of European descent to the intolerable conditions of enslavement. What made race different from other prejudices, including ethnocentrism (the idea that a given culture is superior), is that it claimed that differences were natural, unchanging, and God-given. Eventually, race also received the stamp of science.

Swedish taxonomist Carl Linnaeus divided humanity up into racial categories according to his notion of shared essences among populations, a concept researchers now recognize has no scientific basis. Wikimedia Commons

Over the next decades, Euro-American natural scientists debated the details of race, asking questions such as how often the races were created (once, as stated in the Bible, or many separate times), the number of races, and their defining, essential characteristics. But they did not question whether races were natural things. They reified race, making the idea of race real by unquestioning, constant use.

In the 1700s, Carl Linnaeus, the father of modern taxonomy and someone not without ego, liked to imagine himself as organizing what God created. Linnaeus famously classified our own species into races based on reports from explorers and conquerors.

The race categories he created included Americanus, Africanus, and even Monstrosus (for wild and feral individuals and those with birth defects), and their essential defining traits included a biocultural mlange of color, personality, and modes of governance. Linnaeus described Europeaus as white, sanguine, and governed by law, and Asiaticus as yellow, melancholic, and ruled by opinion. These descriptions highlight just how much ideas of race are formulated by social ideas of the time.

In line with early Christian notions, these racial types were arranged in a hierarchy: a great chain of being, from lower forms to higher forms that are closer to God. Europeans occupied the highest rungs, and other races were below, just above apes and monkeys.

So, the first big problems with the idea of race are that members of a racial group do not share essences, Linnaeus idea of some underlying spirit that unified groups, nor are races hierarchically arranged. A related fundamental flaw is that races were seen to be static and unchanging. There is no allowance for a process of change or what we now call evolution.

There have been lots of efforts since Charles Darwins time to fashion the typological and static concept of race into an evolutionary concept. For example, Carleton Coon, a former president of the American Association of Physical Anthropologists, argued in The Origin of Races (1962) that five races evolved separately and became modern humans at different times.

One nontrivial problem with Coons theory, and all attempts to make race into an evolutionary unit, is that there is no evidence. Rather, all the archaeological and genetic data point to abundant flows of individuals, ideas, and genes across continents, with modern humans evolving at the same time, together.

In this map, darker colors correspond to regions in which people tend to have darker skin pigmentation. Reproduced with permission from Dennis ONeil.

A few pundits such as Charles Murray of the American Enterprise Institute and science writers such as Nicholas Wade, formerly of The New York Times, still argue that even though humans dont come in fixed, color-coded races, dividing us into races still does a decent job of describing human genetic variation. Their position is shockingly wrong. Weve known for almost 50 years that race does not describe human genetic variation.

In 1972, Harvard evolutionary biologist Richard Lewontin had the idea to test how much human genetic variation could be attributed to racial groupings. He famously assembled genetic data from around the globe and calculated how much variation was statistically apportioned within versus among races. Lewontin found that only about 6 percent of genetic variation in humans could be statistically attributed to race categorizations. Lewontin showed that the social category of race explains very little of the genetic diversity among us.

Furthermore, recent studies reveal that the variation between any two individuals is very small, on the order of one single nucleotide polymorphism (SNP), or single letter change in our DNA, per 1,000. That means that racial categorization could, at most, relate to 6 percent of the variation found in 1 in 1,000 SNPs. Put simply, race fails to explain much.

In addition, genetic variation can be greater within groups that societies lump together as one race than it is between races. To understand how that can be true, first imagine six individuals: two each from the continents of Africa, Asia, and Europe. Again, all of these individuals will be remarkably the same: On average, only about 1 out of 1,000 of their DNA letters will be different. A study by Ning Yu and colleagues places the overall difference more precisely at 0.88 per 1,000.

The circles in this diagram represent the relative size and overlap in genetic variation in three human populations. The African population circle (blue) is largest because it contains the most genetic diversity. Genetic diversity in European (orange) and Asian (green) populations is a subset of the variation in Africa. Reproduced by permission of the American Anthropological Association.Adapted from the original, which appeared in the book RACE.Not for sale or further reproduction.

The researchers further found that people in Africa had less in common with one another than they did with people in Asia or Europe. Lets repeat that: On average, two individuals in Africa are more genetically dissimilar from each other than either one of them is from an individual in Europe or Asia.

Homo sapiens evolved in Africa; the groups that migrated out likely did not include all of the genetic variation that built up in Africa. Thats an example of what evolutionary biologists call the founder effect, where migrant populations who settle in a new region have less variation than the population where they came from.

Genetic variation across Europe and Asia, and the Americas and Australia, is essentially a subset of the genetic variation in Africa. If genetic variation were a set of Russian nesting dolls, all of the other continental dolls pretty much fit into the African doll.

What all these data show is that the variation that scientistsfrom Linnaeus to Coon to the contemporary osteoporosis researcherthink is race is actually much better explained by a populations location. Genetic variation is highly correlated to geographic distance. Ultimately, the farther apart groups of people are from one another geographically, and, secondly, the longer they have been apart, can together explain groups genetic distinctions from one another. Compared to race, those factors not only better describe human variation, they invoke evolutionary processes to explain variation.

Those osteoporosis doctors might argue that even though socially defined race poorly describes human variation, it still could be a useful classification tool in medicine and other endeavors. When the rubber of actual practice hits the road, is race a useful way to make approximations about human variation?

When Ive lectured at medical schools, my most commonly asked question concerns sickle cell trait. Writer Sherman Alexie, a member of the Spokane-Coeur dAlene tribes, put the question this way in a 1998 interview: If race is not real, explain sickle cell anemia to me.

In sickle cell anemia, red blood cells take on an unusual crescent shape that makes it harder for the cells to pass through small blood vessels. Mark Garlick/Science Photo Library/AP Images

OK! Sickle cell is a genetic trait: It is the result of an SNP that changes the amino acid sequence of hemoglobin, the protein that carries oxygen in red blood cells. When someone carries two copies of the sickle cell variant, they will have the disease. In the United States, sickle cell disease is most prevalent in people who identify as African American, creating the impression that it is a black disease.

Yet scientists have known about the much more complex geographic distribution of sickle cell mutation since the 1950s. It is almost nonexistent in the Americas, most parts of Europe and Asiaand also in large swaths of Northern and Southern Africa. On the other hand, it is common in West-Central Africa and also parts of the Mediterranean, Arabian Peninsula, and India. Globally, it does not correlate with continents or socially defined races.

In one of the most widely cited papers in anthropology, American biological anthropologist Frank Livingstone helped to explain the evolution of sickle cell. He showed that places with a long history of agriculture and endemic malaria have a high prevalence of sickle cell trait (a single copy of the allele). He put this information together with experimental and clinical studies that showed how sickle cell trait helped people resist malaria, and made a compelling case for sickle cell trait being selected for in those areas. Evolution and geography, not race, explain sickle cell anemia.

What about forensic scientists: Are they good at identifying race? In the U.S., forensic anthropologists are typically employed by law enforcement agencies to help identify skeletons, including inferences about sex, age, height, and race. The methodological gold standards for estimating race are algorithms based on a series of skull measurements, such as widest breadth and facial height. Forensic anthropologists assume these algorithms work.

Skull measurements are a longstanding tool in forensic anthropology. Internet Archive Book Images/Flickr

The origin of the claim that forensic scientists are good at ascertaining race comes from a 1962 study of black, white, and Native American skulls, which claimed an 8090 percent success rate. That forensic scientists are good at telling race from a skull is a standard trope of both the scientific literature and popular portrayals. But my analysis of four later tests showed that the correct classification of Native American skulls from other contexts and locations averaged about two incorrect for every correct identification. The results are no better than a random assignment of race.

Thats because humans are not divisible into biological races. On top of that, human variation does not stand still. Race groups are impossible to define in any stable or universal way. It cannot be done based on biologynot by skin color, bone measurements, or genetics. It cannot be done culturally: Race groupings have changed over time and place throughout history.

Science 101: If you cannot define groups consistently, then you cannot make scientific generalizations about them.

Wherever one looks, race-as-genetics is bad science. Moreover, when society continues to chase genetic explanations, it misses the larger societal causes underlying racial inequalities in health, wealth, and opportunity.

To be clear, what I am saying is that human biogenetic variation is real. Lets just continue to study human genetic variation free of the utterly constraining idea of race. When researchers want to discuss genetic ancestry or biological risks experienced by people in certain locations, they can do so without conflating these human groupings with racial categories. Lets be clear that genetic variation is an amazingly complex result of evolution and mustnt ever be reduced to race.

Similarly, race is real, it just isnt genetic. Its a culturally created phenomenon. We ought to know much more about the process of assigning individuals to a race group, including the category white. And we especially need to know more about the effects of living in a racialized world: for example, how a societys categories Race is real, it just isnt genetic. Its a culturally created phenomenon.and prejudices lead to health inequalities. Lets be clear that race is a purely sociopolitical construction with powerful consequences.

It is hard to convince people of the dangers of thinking race is based on genetic differences. Like climate change, the structure of human genetic variation isnt something we can see and touch, so it is hard to comprehend. And our culturally trained eyes play a trick on us by seeming to see race as obviously real. Race-as-genetics is even more deeply ideologically embedded than humanitys reliance on fossil fuels and consumerism. For these reasons, racial ideas will prove hard to shift, but it is possible.

Over 13,000 scientists have come together to formand publicizea consensus statement about the climate crisis, and that has surely moved public opinion to align with science. Geneticists and anthropologists need to do the same for race-as-genetics. The recent American Association of Physical Anthropologists Statement on Race & Racism is a fantastic start.

In the U.S., slavery ended over 150 years ago and the Civil Rights Law of 1964 passed half a century ago, but the ideology of race-as-genetics remains. It is time to throw race-as-genetics on the scrapheap of ideas that are no longer useful.

We can start by getting my friendand anyone else who has been deniedthat long-overdue bone density test.

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Race Is Real, But It's Not Genetic - SAPIENS

Genomics took a long time to fulfil its promise – The Economist

Mar 12th 2020

THE ATOMIC bomb convinced politicians that physics, though not readily comprehensible, was important, and that physicists should be given free rein. In the post-war years, particle accelerators grew from the size of squash courts to the size of cities, particle detectors from the scale of the table top to that of the family home. Many scientists in other disciplines looked askance at the money devoted to this big science and the vast, impersonal collaborations that it brought into being. Some looked on in envy. Some made plans.

The idea that sequencing the whole human genome might provide biology with some big science of its own first began to take root in the 1980s. In 1990 the Human Genome Project was officially launched, quickly growing into a global endeavour. Like other fields of big science it developed what one of the programmes leaders, the late John Sulston, called a tradition of hyperbole. The genome was Everest; it was the Apollo programme; it was the ultimate answer to that Delphic injunction, know thyself. And it was also, in prospect, a cornucopia of new knowledge, new understanding and new therapies.

By the time the completion of a (rather scrappy) draft sequence was announced at the White House in 2000, even the politicians were drinking the Kool-Aid. Tony Blair said it was the greatest breakthrough since antibiotics. Bill Clinton said it would revolutionise the diagnosis, prevention and treatment of most, if not all, human diseases. In coming years, doctors increasingly will be able to cure diseases like Alzheimers, Parkinsons, diabetes and cancer by attacking their genetic roots.

Such hype was always going to be hard to live up to, and for a long time the genome project failed comprehensively, prompting a certain Schadenfreude among those who had wanted biology kept small. The role of genetics in the assessment of peoples medical futures continued to be largely limited to testing for specific defects, such as the BRCA1 and BRCA2 mutations which, in the early 1990s, had been found to be responsible for some of the breast cancers that run in families.

To understand the lengthy gap between the promise and the reality of genomics, it is important to get a sense of what a genome really is. Although sequencing is related to an older technique of genetic analysis called mapping, it produces something much more appropriate to the White House kitchens than to the Map Room: a recipe. The genes strung out along the genomes chromosomesbig molecules of DNA, carefully packedare descriptions of lifes key ingredients: proteins. Between the genes proper are instructions as to how those ingredients should be used.

If every gene came in only one version, then that first human genome would have been a perfect recipe for a person. But genes come in many varietiesjust as chilies, or olive oils, or tinned anchovies do. Some genetic changes which are simple misprints in the ingredients specification are bad in and of themselvesjust as a meal prepared with fuel oil instead of olive oil would be inedible. Others are problematic only in the context of how the whole dish is put together.

The most notorious of the genes with obvious impacts on health were already known before the genome was sequenced. Thus there were already tests for cystic fibrosis and Huntingtons disease. The role of genes in common diseases turned out to be a lot more involved than many had naively assumed. This made genomics harder to turn into useful insight.

Take diabetes. In 2006 Francis Collins, then head of genome research at Americas National Institutes of Health, argued that there were more genes involved in diabetes than people thought. Medicine then recognised three such genes. Dr Collins thought there might be 12. Today the number of genes with known associations to type-2 diabetes stands at 94. Some of these genes have variants that increase a persons risk of the disease, others have variants that lower that risk. Most have roles in various other processes. None, on its own, amounts to a huge amount of risk. Taken together, though, they can be quite predictivewhich is why there is now an over-the-counter genetic test that measures peoples chances of developing the condition.

In the past few years, confidence in sciences ability to detect and quantify such genome-wide patterns of susceptibility has increased to the extent that they are being used as the basis for something known as a polygenic risk score (PRS). These are quite unlike the genetic tests people are used to. Those single-gene tests have a lot of predictive value: a person who has the Huntingtons gene will get Huntingtons; women with a dangerous BRCA1 mutation have an almost-two-in-three chance of breast cancer (unless they opt for a pre-emptive mastectomy). But the damaging variations they reveal are rare. The vast majority of the women who get breast cancer do not have BRCA mutations. Looking for the rare dangerous defects will reveal nothing about the other, subtler but still possibly relevant genetic traits those women do have.

Polygenic risk scores can be applied to everyone. They tell anyone how much more or less likely they are, on average, to develop a genetically linked condition. A recently developed PRS for a specific form of breast cancer looks at 313 different ways that genomes vary; those with the highest scores are four times more likely to develop the cancer than the average. In 2018 researchers developed a PRS for coronary heart disease that could identify about one in 12 people as being at significantly greater risk of a heart attack because of their genes.

Some argue that these scores are now reliable enough to bring into the clinic, something that would make it possible to target screening, smoking cessation, behavioural support and medications. However, hope that knowing their risk scores might drive people towards healthier lifestyles has not, so far, been validated by research; indeed, so far things look disappointing in that respect.

Assigning a PRS does not require sequencing a subjects whole genome. One just needs to look for a set of specific little markers in it, called SNPs. Over 70,000 such markers have now been associated with diseases in one way or another. But if sequencing someones genome is not necessary in order to inspect their SNPs, understanding what the SNPs are saying in the first place requires that a lot of people be sequenced. Turning patterns discovered in the SNPs into the basis of risk scores requires yet more, because you need to see the variations in a wide range of people representative of the genetic diversity of the population as a whole. At the moment people of white European heritage are often over-represented in samples.

The first genome cost, by some estimates, $3bn

The need for masses of genetic information from many, many human genomes is one of the main reasons why genomic medicine has taken off rather slowly. Over the course of the Human Genome Project, and for the years that followed, the cost of sequencing a genome fell quicklyas quickly as the fall in the cost of computing power expressed through Moores law. But it was falling from a great height: the first genome cost, by some estimates, $3bn. The gap between getting cheaper quickly and being cheap enough to sequence lots of genomes looked enormous.

In the late 2000s, though, fundamentally new types of sequencing technology became available and costs dropped suddenly (see chart). As a result, the amount of data that big genome centres could produce grew dramatically. Consider John Sulstons home base, the Wellcome Sanger Institute outside Cambridge, England. It provided more sequence data to the Human Genome Project than any other laboratory; at the time of its 20th anniversary, in 2012, it had produced, all told, almost 1m gigabytesone petabyteof genome data. By 2019, it was producing that same amount every 35 days. Nor is such speed the preserve of big-data factories. It is now possible to produce billions of letters of sequence in an hour or two using a device that could easily be mistaken for a chunky thumb drive, and which plugs into a laptop in the same way. A sequence as long as a human genome is a few hours work.

As a result, thousands, then tens of thousands and then hundreds of thousands of genomes were sequenced in labs around the world. In 2012 David Cameron, the British prime minister, created Genomics England, a firm owned by the government, and tasked initially with sequencing 100,000 genomes and integrating sequencing, analysis and reporting into the National Health Service. By the end of 2018 it had finished the 100,000th genome. It is now aiming to sequence five million. Chinas 100,000 genome effort started in 2017. The following year saw large-scale projects in Australia, America and Turkey. Dubai has said it will sequence all of its three million residents. Regeneron, a pharma firm, is working with Geisinger, a health-care provider, to analyse the genomes of 250,000 American patients. An international syndicate of investors from America, China, Ireland and Singapore is backing a 365m ($405m) project to sequence about 10% of the Irish population in search of disease genes.

Genes are not everything. Controls on their expressionepigentics, in the jargonand the effects of the environment need to be considered, too; the kitchen can have a distinctive effect on the way a recipe turns out. That is why biobanks are being funded by governments in Britain, America, China, Finland, Canada, Austria and Qatar. Their stores of frozen tissue samples, all carefully matched to clinical information about the person they came from, allow study both by sequencing and by other techniques. Researchers are keen to know what factors complicate the lines science draws from genes to clinical events.

Today various companies will sequence a genome commercially for $600-$700. Sequencing firms such as Illumina, Oxford Nanopore and Chinas BGI are competing to bring the cost down to $100. In the meantime, consumer-genomics firms will currently search out potentially interesting SNPs for between $100 and $200. Send off for a home-testing kit from 23andMe, which has been in business since 2006, and you will get a colourful box with friendly letters on the front saying Welcome to You. Spit in a test tube, send it back to the company and you will get inferences as to your ancestry and an assessment of various health traits. The health report will give you information about your predisposition to diabetes, macular degeneration and various other ailments. Other companies offer similar services.

Plenty of doctors and health professionals are understandably sceptical. Beyond the fact that many gene-testing websites are downright scams that offer bogus testing for intelligence, sporting ability or wine preference, the medical profession feels that people are not well equipped to understand the results of such tests, or to deal with their consequences.

An embarrassing example was provided last year by Matt Hancock, Britains health minister. In an effort to highlight the advantages of genetic tests, he revealed that one had shown him to be at heightened risk of prostate cancer, leading him to get checked out by his doctor. The test had not been carried out by Britains world-class clinical genomics services but by a private company; critics argued that Mr Hancock had misinterpreted the results and consequently wasted his doctors time.

23andMe laid off 14% of its staff in January

He would not be the first. In one case, documented in America, third-party analysis of genomic data obtained through a website convinced a woman that her 12-year-old daughter had a rare genetic disease; the girl was subjected to a battery of tests, consultations with seven cardiologists, two gynaecologists and an ophthalmologist and six emergency hospital visits, despite no clinical signs of disease and a negative result from a genetic test done by a doctor.

At present, because of privacy concerns, the fortunes of these direct-to-consumer companies are not looking great. 23andMe laid off 14% of its staff in January; Veritas, which pioneered the cheap sequencing of customers whole genomes, stopped operating in America last year. But as health records become electronic, and health advice becomes more personalised, having validated PRS scores for diabetes or cardiovascular disease could become more useful. The Type 2 diabetes report which 23andMe recently launched looks at over 1,000 SNPs. It uses a PRS based on data from more than 2.5m customers who have opted to contribute to the firms research base.

As yet, there is no compelling reason for most individuals to have their genome sequenced. If genetic insights are required, those which can be gleaned from SNP-based tests are sufficient for most purposes. Eventually, though, the increasing number of useful genetic tests may well make genome sequencing worthwhile. If your sequence is on file, many tests become simple computer searches (though not all: tests looking at the wear and tear the genome suffers over the course of a lifetime, which is important in diseases like cancer, only make sense after the damage is done). If PRSs and similar tests come to be seen as valuable, having a digital copy of your genome at hand to run them on might make sense.

Some wonder whether the right time and place to do this is at birth. In developed countries it is routine to take a pinprick of blood from the heel of a newborn baby and test it for a variety of diseases so that, if necessary, treatment can start quickly. That includes tests for sickle-cell disease, cystic fibrosis, phenylketonuria (a condition in which the body cannot break down phenylalanine, an amino acid). Some hospitals in America have already started offering to sequence a newborns genome.

Sequencing could pick up hundreds, or thousands, of rare genetic conditions. Mark Caulfield, chief scientist at Genomics England, says that one in 260 live births could have a rare condition that would not be spotted now but could be detected with a whole-genome sequence. Some worry, though, that it would also send children and parents out of the hospital with a burden of knowledge they might be better off withoutespecially if they conclude, incorrectly, that genetic risks are fixed and predestined. If there is unavoidable suffering in your childs future do you want to know? Do you want to tell them? If a child has inherited a worrying genetic trait, should you see if you have it yourselfor if your partner has? The ultimate answer to the commandment know thyself may not always be a happy one.

This article appeared in the Technology Quarterly section of the print edition under the headline "Welcome to you"

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Genomics took a long time to fulfil its promise - The Economist