#COVID-19 Genomics UK Consortium

[covid-safer-hotties]

Impact of vaccination on SARS-CoV-2 transmission in the UK: a modelling study - Preprint Posted Sept 7, 2024

An interesting preprint. TL;DR: Vaccination for covid in-and-of itself does little to halt the spread. We must take further measures such as masking, testing, distancing when ill, and improving ventilation/air quality indoors.

Abstract Background Efficacy and effectiveness of vaccines against SARS-CoV-2 infection, severe disease and death have been widely assessed. However, the impact of vaccination against SARS-CoV-2 transmission is far less well-characterized, and has major implications for public health, because it informs the indirect effects of vaccination in addition to its direct effects. Analysing the effects of SARS-CoV-2 vaccination on transmission is challenging, because they must be considered in tandem with the time-varying reproduction number (Rt), while also accounting for regional variability, for example due to the presence of more transmissible variants.

Methods We fitted a Bayesian hierarchical model to previously obtained estimates of Rt to estimate the effectiveness of vaccination with one, two and three doses on SARS-CoV-2 transmission in the UK during 2021. Vaccine effectiveness is defined as the proportional reduction in the time-varying reproduction number Rt. The model accounts for transmission at national and Lower Tier Local Authority (LTLA)-level, and uses vaccination data provided by the UK Health Security Agency (UKHSA), detailing the LTLA-specific proportions of people who have received doses one, two and three. The model also incorporates data on the proportion of wild-type, Alpha and Delta SARS-CoV-2 variants over time in each LTLA, obtained from UKHSA and the COVID-19 Genomics UK (COG-UK) Consortium.

Results We find that vaccination had moderate-to-large effectiveness against transmission for dose 1 (39.30%, 95% CrI 26.64% - 48.07%), and for dose 3 (48.69%, 95% CrI 27.97% - 71.30%), but negligible effects on dose 2, likely attributable to the coincident importation and dominance of the Delta variant in the UK. Nationally, our model fitted the previously estimated values of time-series of Rt values well, largely reproducing the reproduction number averaged across LTLAs for each timepoint. This lends support to our hypothesis that the extent of vaccination (or lack thereof) was a major determinant of transmission intensity. Our model fits further reproduced well the reproduction numbers at regional level, although outliers were less well captured, implying some degree of variation that is not explained by our model.

Conclusions To our knowledge, our analysis is the first evidence of the effectiveness of SARS-CoV-2 vaccination against its transmission at population level. We find that vaccination is an effective tool for the control of SARS-CoV-2 transmission, in addition to its well-documented effects on disease burden and mortality. Our results allow future assessment of the impact of vaccination accounting for several circulating variants and sociodemographic factors.

[newswireml]

Keep scientists in the research room and out of politics | Fiona Fox#scientists #research #room #politics #Fiona #Fox

Matt Hancock’s views about the independent experts advising government, detailed in the Lockdown Files, are revealing. They were “totally unreliable” and “wacky” (Dame Kate Bingham); a “totally offside… loudmouth” (Sir Jeremy Farrar); and a “prize idiot” (Prof Jon Deeks); while Prof Sharon Peacock, the amazing scientist who set up Covid-19 Genomics UK Consortium (COG-UK), was deemed “a total…

[rpnewspaperblog]

Keep scientists in the research room and out of politics | Fiona Fox

Matt Hancock’s views about the independent experts advising government, detailed in the Lockdown Files, are revealing. They were “totally unreliable” and “wacky” (Dame Kate Bingham); a “totally offside… loudmouth” (Sir Jeremy Farrar); and a “prize idiot” (Prof Jon Deeks); while Prof Sharon Peacock, the amazing scientist who set up Covid-19 Genomics UK Consortium (COG-UK), was deemed “a total…

[eagletek]

Keep scientists in the research room and out of politics | Fiona Fox

Matt Hancock’s views about the independent experts advising government, detailed in the Lockdown Files, are revealing. They were “totally unreliable” and “wacky” (Dame Kate Bingham); a “totally offside… loudmouth” (Sir Jeremy Farrar); and a “prize idiot” (Prof Jon Deeks); while Prof Sharon Peacock, the amazing scientist who set up Covid-19 Genomics UK Consortium (COG-UK), was deemed “a total…

[newsfromtherooftop]

The hidden lives of the women scientists who tackled COVID-19

The hidden lives of the women scientists who tackled COVID-19 l New book tells personal stories of women scientists. #COVID-19 #UniversityofPortsmouth #Women

Researchers from the University of Portsmouth, have been recognised for their scientific excellence during the COVID-19 pandemic in a new book. ‘Snapshots of Women in COG: Scientific excellence during the COVID-19 pandemic’ has been published by the UK’s COVID-19 Genomics UK (COG-UK) Consortium.  The book tells personal stories from women involved in the COVID-19 pandemic and is a celebration…

[hummingzone]

Coronavirus live updates | Delhi High Court quashes GST on oxygen concentrators

Coronavirus live updates | Delhi High Court quashes GST on oxygen concentrators

India ought to realistically expect around a 1.3 billion doses of vaccines from August to December and not the 2 billion that the Centre has projected, said epidemiologist, public health expert and author Dr. Chandrakant Lahariya, in an interview to The Hindu. Dr. Lahariya, who was formerly with the World Health Organisation, said that there was no evidence so far that a potential third wave…

[ds4techofficial]

Coronavirus live updates | UN chief blasts vaccine nationalism

Coronavirus live updates | UN chief blasts vaccine nationalism

India’s indigenous COVID-19 vaccine Covaxin from Hyderabad-based Bharat Biotechis now authorised for emergency use on a par with Oxford-AstraZeneca’s Covishield, NITI Aayog’s member (health) V.K. Paul said on Thursday. India is now seeing a rise in the number of active cases after touching lowest mark in mid-February. Haryana, Gujarat, Madhya Pradesh, Punjab and Maharashtra are the top States…

[antoine-roquentin]

NERVTAG gave no details about where in Kent the variant was first located, but the Covid-19 Genomics UK Consortium said that a key sample came from a patient living ‘near Canterbury’. A medical source, who wanted to stay anonymous, told me that the variant was first identified in Margate and came from someone with a weak immune system. Some in Kent jibbed at the prospect that the new virus would be known to history as ‘the Kent variant’, drawing a parallel with Trump’s ‘China virus’ or the ‘Spanish flu’ that didn’t even come from Spain (it first reached epidemic level in military training camps in the US).

It would be difficult to find a place where coronavirus was more likely to flourish and to enhance its mode of attack than Thanet and Swale. As in much of coastal Britain, few of the towns here are still working ports or seaside resorts. What industry there once was is largely gone, taking with it the few well-paying jobs. Of the fifteen most deprived neighbourhoods in Kent, seven are in Thanet and six in Swale. ‘We lost the mining industry and Ramsgate harbour, which was a big employer,’ the Labour councillor Barry Lewis says, lamenting the repeated blows to Margate over the past forty years. The hotel and tourism industries collapsed ‘when everybody started going abroad for their holidays’. The last big manufacturer in the area was the Pfizer plant near Sandwich, which closed in 2011 with the loss of 1500 jobs. The jobs that remain are often on zero-hours contracts. A map showing areas of maximum deprivation fitted neatly over one showing high rates of viral infection.

Everything about the average working life of someone in Swale or Sheppey puts them at risk. Much of this is to do with the need to go out to work. As Jackie Cassell, a public health specialist at the Brighton and Sussex Medical School who grew up on Sheppey, put it, ‘poverty is a mechanism for increasing social contact.’ People on the island are more likely than the population at large to use public transport to get to work, doing shifts of eight or more hours a day in warehouses or on construction sites. And people with little money are more likely to look after sick or ageing relatives. In a study of working patterns, Cassell found that on average someone who goes out to work has twelve prolonged or close periods of contact with people and seventeen brief or distant ones; those working from home have only two close or prolonged periods of contact and two brief or distant ones.

The effect this has in practice depends on the nature of the job and the employer. Riddell, the railway conductor and trade union official, says that the proportion of train passengers wearing face masks varies from line to line, but the stretch from Sittingbourne to Sheerness on the west side of Sheppey is particularly risky for rail staff because ‘between 50 and 60 per cent of people, mostly the young ones, don’t wear masks.’ As a conductor, he is allowed stay in the front cabin with the driver and doesn’t have to check passengers’ tickets. But Sue Saunders, who works as a cleaner on the trains, has to walk through the carriages spraying sanitiser and cleaning surfaces. ‘We have visors, masks and gloves,’ she says, ‘but we fear for our safety and several of my friends have caught Covid.’ The cleaners are often the only official-looking people on a train and, according to Saunders, are frequently stopped by passengers who want information. She says that sanitising could be done when the trains are standing empty between journeys, but the train companies want passengers to see that the cleaners are at work.

Compliance with restrictions on social interaction largely lapsed over the summer. Sharon Goodyer, who runs the Margate Food Club, says that her volunteers sometimes couldn’t safely distribute food in poor areas because they had to push past people sitting in doorways and mixing in the street. ‘I have a feeling,’ she says, ‘that if this new variant started in Margate, then we earned it.’ But she points out that even poor people need to get outdoors: ‘You can’t be too judgmental if you’re living in a nice house and don’t have mice dying under your chair.’ Barry Lewis mentions one street in Margate with two hundred overcrowded houses where residents rent tiny rooms at high prices. ‘It’s almost a prison, so to get out to the front of the house is your normal way of life and to be stuck in one overcrowded room is not possible.’

The arrival of the variant changed attitudes. Vanessa Crick, a mother of three in Herne Bay, a rundown town on the coast between Swale and Thanet, has two jobs, in the local library and in a supermarket. ‘Since last November,’ she says, ‘more people have started wearing masks because they are frightened for their granddad or their nan.’ Charlotte Cornell, who runs a charity distributing laptops for homeschooling to children in deprived areas, says that none of the families she deals with is cavalier about the virus: ‘They are all terrified of it.’

When public health experts were sent to Kent at the end of last year to investigate the reasons for the local epidemic, they suspected that the spread would be attributable to human actions at home or in the workplace. Everything they knew about the lives of people in Thanet and Swale would favour accelerated transmission of the virus. The physical environment was a factor too: decayed seaside resorts have many former hotels with sea views whose faded grandeur make them ideal for conversion into care homes. Last May, seventeen residents died from Covid-19 in one such care home in Margate, but mass deaths in care homes were a scandal all over Britain and hardly peculiar to Thanet.

A more likely reason for the rapid spread is that many people had good reasons for not getting Covid tests. People who test positive but need to go out to work and won’t get sick pay can’t afford to quarantine. ‘Young males in economically deprived areas do not want to get tested,’ Jackie Cassell says of Swale. She points to a study in Liverpool where only 4 per cent of people in one of the city’s poorest neighbourhoods volunteered for a test. Since the pandemic began, the government has been voluble about the restrictions it has imposed but evasive about how far people comply with them. A study by King’s College London showed that, while 70 per cent of people said they would self-isolate if necessary, only 18 per cent did so.

People not getting tested because they can’t afford to quarantine will keep a low profile. But other groups aren’t keen to catch the attention of anyone in authority. Graham Tegg, the director of the Kent Law Clinic, which provides free legal assistance, says there is ‘an underground system’ of migrant workers, many of whom have lived in Britain for a long time, who want to keep their distance from state institutions. Many of his clients are Czechs, Poles and Roma. Some pick fruit and vegetables or work in packing factories; collected by minivans in the morning, they work for ten hours and come back in the evening in the same van. ‘Three or four of them may be living in the same small room,’ Tegg says, providing perfect conditions for the virus to spread.

But most people in Thanet and Swale are ‘disconnected from authority’, according to Barry Lewis: the only time they see authority in action is when the police stop them doing something they want to do. Some of them are third-generation unemployed whose only prospect for making money is in the black market or the drugs trade – described by one resident as the only growth industry in Thanet. ‘What we have here is a whole community who have no investment in society at all,’ Sharon Goodyer says. ‘What do they owe anybody? They don’t. They don’t have a decent education, a decent home, a decent job. Why should they behave responsibly?’

[bestitmagazine]

Technology Magazine Indian

Technology Magazine Indian SARS-CoV-2 Consortium on Genomics (INSACOG) is a grouping of 10 National Laboratories that was established by Ministry of Health and Family Welfare, Govt of India on 25/12/2020. INSACOG is since then carrying out genomic sequencing and analysis of circulating COVID-19 viruses, and correlating epidemiological trends with genomic variants. Genomic variants of various viruses are a natural phenomenon and are found in almost all countries. Since INSACOG initiated its work, 771 variants of concerns (VOCs) have been detected in a total of 10787 positive samples shared by States/UTs. These include 736 samples positive for viruses of the UK (B.1.1.7) lineage. 34 samples were found positive for viruses of the South African (B.1.351) lineage.  1 sample was found positive for viruses of the Brazilian (P.1) lineage. The samples with these VOCs have been identified in 18 States of the country. Visit on varindia site to know more about it https://www.varindia.com/

[innocentamit]

Look at the full vaccine: Hindu editor at the speed of the Indian vaccine COVID-19

Look at the full vaccine: Hindu editor at the speed of the Indian vaccine COVID-19

Although a slight increase in new daily cases was reported in November, the Indian SARS-CoV-2 Genomics Consortium (INSACOG) said no new types of interest or concern had been identified in India. And other changes besides the Delta one now “are useless in filtering data from India”. AY4.2, a type of Delta, which is growing slowly according to lawsuits reported in the UK, states, “innumerable” in…

[bestweb20sitelist]

The quest to find genes that drive severe COVID

New Post has been published on https://uspost.xyz/uncategorized/the-quest-to-find-genes-that-drive-severe-covid/

The quest to find genes that drive severe COVID

Since last March, research teams around the world have scoured the genomes of more than 100,000 people with COVID-19, hoping to find genetic clues to who will be hit hardest by an infection with the virus SARS-CoV-2. What’s emerged from this effort is a dozen or so genetic variants that have a strong statistical association with a person’s chances of developing COVID-19 and becoming gravely ill with the disease, the teams report in a summary analysis published on 8 July in Nature1.

“There were actually quite a few very common genetic variants that were really important in COVID-19,” says Guillaume Butler-Laporte, an infectious-disease physician and genetic epidemiologist at McGill University in Montreal, Canada. “I don’t think we expected to find them so clearly.”

The loosely aligned teams involved in the analysis include both academic laboratories and private firms such as the US companies 23andMe and AncestryDNA, and have been releasing their work steadily over the past year. Known collectively as the COVID-19 Host Genetics Initiative (HGI), they first posted their summary — an amalgamation of 46 separate studies covering, at the time of analysis, almost 50,000 people with COVID-19 — on the medRxiv preprint server in March.

The genetic associations they found increase risk by a relatively small amount, although some of the rises are comparable to those for risk factors such as obesity, diabetes and other underlying health conditions (see ‘Genetic variants that change COVID-19 risk’).

But the findings can shed light on biological mechanisms of the disease, and suggest which drugs to test, says Kenneth Baillie, an intensive-care physician and a geneticist at the University of Edinburgh, UK. In other research, scientists have also picked out rare genetic mutations — in contrast to the relatively common variants listed in the latest HGI study — that might also explain the root causes of severe disease.

Not everyone is convinced that the genetic work gives immediate insight. “We’re starting to get a pretty good genetic map,” says Julian Knight, a human geneticist at the University of Oxford, UK. “To move that on to where we’ve got good drug targets or an understanding of disease variability, that’s going to be a big step.” This, he says, is a typical issue for research that tries to link common variations in genomes with people’s risk of complex diseases.

And Kári Stefánsson, chief executive of deCODE Genetics in Reykjavik and a member of the HGI, doesn’t feel that the work to find genetic ‘hits’ has been especially fruitful — at least so far. Still, Stefánsson says, “I think it’s extremely important to follow as many of these as possible. You may be able to find a mechanism of major importance.”

Although geneticists don’t yet have all the answers, they’ve moved extremely rapidly to unpick associations with COVID-19, says Brent Richards, a geneticist and endocrinologist at McGill University who is part of the HGI. “The human-genetics community hasn’t slept much this year,” he says.

Genetic hits for COVID-19

The HGI worked less like a consortium focused on a single unifying project, and more as a clearing house for collaborations, support and advice. Teams were free to publish their own studies, while contributing to pooled studies that combined individual efforts. “It was just a matter of creating a place that people would feel comfortable together, and work together,” says Andrea Ganna, a statistical geneticist who co-founded the HGI with geneticist Mark Daly; both are at the University of Helsinki and the Broad Institute in Cambridge, Massachusetts.

Ganna is a specialist in genome-wide association studies (GWAS) — the bread and butter of genetic epidemiology. These examine hundreds of thousands of relatively common single-letter DNA differences across the genome in large numbers of people, to see whether any are enriched in people with a particular disease or trait. It was inevitable that people would apply GWAS to COVID-19, Ganna says.

One genomic variant identified by Baillie’s team and confirmed in other HGI efforts is near a family of antiviral genes called OAS (oligoadenylate synthase). The genes activate enzymes that chew up viral RNA, and HGI studies1,2 show that a variant that leads to lower circulating levels of the OAS1 enzyme in the lungs increases risk of infection, hospitalization and critical illness. Most coronaviruses counteract this protection using proteins called PDEs, or phosphodiesterases, but SARS-CoV-2 doesn’t make PDEs. “So this might provide an Achilles heel,” explains Richards, who is aware of pharmaceutical companies that are pursuing the target, but declines to reveal details. On the basis of the genetic association, drugs known as phosphodiesterase 12 inhibitors are predicted to boost natural antiviral defences, Baillie says.

Another variant spotted by Baillie’s team and confirmed in other COVID-19 GWAS is near a gene that encodes a portion of a cellular receptor for molecules called interferons1, which are well known for boosting people’s immune responses to viruses. Because of this antiviral role, one kind of interferon molecule had already been tested in trials, before the genetic association came to light. It was one of the first drugs included in the World Health Organization-sponsored ‘Solidarity’ trial of COVID-19 treatments, but didn’t help patients. It’s possible that the genetic prediction was wrong, Baillie says, but it could be that interferon needs to be administered earlier in infection, or in a different manner to the subcutaneous or intravenous injections that Solidarity trial participants received.

Baillie also says that other genetic associations are now being used to prioritize treatments. One example is in the widely praised UK-based RECOVERY trial, which most famously showed the benefit of a common steroid for people with severe COVID-193. The trial is using genetic data to help select drugs to test — including a rheumatoid arthritis drug called baricitinib and a treatment for psoriasis and multiple sclerosis called dimethyl fumarate, says Baillie, who is part of the effort.

Baricitinib inhibits the protein encoded by a gene, TYK2, that was associated with life-threatening COVID-192. The relationship between TYK2 activity and risk of severe COVID-19 isn’t clear-cut from the genetic studies, “but it did provide a big extra source of support for the idea”, says Baillie. Dimethyl fumarate was included largely for its known role in quelling an inflammatory process involved in severe COVID-19, but genetic links provided added support for testing it in RECOVERY, says Baillie.

GWAS, however, also have a reputation for delivering head-scratching results. That has happened with COVID-19, too: the strongest association between any gene variant and severe COVID-19 lies in a poorly studied region of chromosome 31. “We still don’t quite know, as a scientific community, why it’s so important,” says Butler-Laporte. The chromosome 3 region includes several genes involved in immune signalling, lung biology and other plausible mechanisms. But it’s not clear which of these genes explains the association with COVID-19.

People who carry this gene variant are around twice as likely as others to be hospitalized with COVID-19. A study4 led by Richards, Ganna and Tomoko Nakanishi, a geneticist and respiratory physician at McGill, found that the variant raises the odds of people aged 60 or under becoming critically ill or dying from COVID-19 as much as and perhaps even more than risk factors including diabetes, obesity and chronic obstructive pulmonary disease.

Risk scores

As a result of such associations, some researchers are exploring whether the genetic links turned up in GWAS could be used to predict an individual’s risk of a life-threatening SARS-CoV-2 infection. Risk scores, which amalgamate associations discovered in GWAS, have been used to measure an individual’s risk of conditions such as type 2 diabetes, various cancers and cardiovascular disease.

But it’s not clear whether this approach could work for COVID-19 — or is even needed, given the availability of vaccines. In June, a firm in Fitzroy, Australia, called Genetic Technologies launched a US$175 test to predict people’s risk of developing severe COVID-19. But it also relies on age, sex and health, all factors that significantly improve the predictive power of the GWAS associations5.

Chief scientific officer Richard Allman says that the firm’s test, which was developed and validated using data from the UK Biobank database, might be most useful for middle-aged people. Most will have a relatively small risk of severe COVID-19, but the test could identify those rare individuals with vastly increased (or dramatically reduced) chances of developing a life-threatening infection. The firm’s test is currently available only in the United States, through a company called Infinity BiologiX in Piscataway, New Jersey, and with consultation from a health professional. Still, Genetic Technologies is in talks with companies interested in offering the test to employees, says Allman, who says he does not have sales figures.

Nakanishi, Richards and Ganna say that it’s not clear whether the test has been validated enough to be reliable, but that that doesn’t mean such tests couldn’t be useful as another motivation for higher-risk people to get vaccinated. “It might get a few people over the edge who are worried [about vaccination],” adds Genetic Technologies biostatistician Gillian Dite.

Genetic studies of COVID-19 — like those of most other diseases — have overwhelmingly been based on people with European ancestry. That’s a problem, says Knight, because of the global burden of COVID-19 and elevated rates of disease in minority ethnic groups in countries such as the United States and United Kingdom. “We really need to make the investment in genetics in those populations.”

Diversifying genetic studies can not only improve understanding of risk variants identified in European populations, but also identify new ones in other groups. A GWAS that included more than 2,000 people hospitalized with COVID-19 in Japan6 identified many of the variants flagged by studies of European populations, as well as an immune gene, called DOCK2, with a role in interferon production that hadn’t come up in other studies. The DOCK2 variant that increased COVID-19 risk was relatively common in East Asians, but very rare in people of European, South Asian and African ancestry. “This tells us the importance of increasing diversity in host genetics of COVID-19,” says study leader Yukinori Okada, a statistical geneticist at Osaka University in Japan.

Rare mutations

Some researchers feel that the GWAS approach, which has found common variants that raise an individual’s risk only by a small amount, is less fruitful than spotting much rarer mutations that might explain why some otherwise healthy people are in intensive care with COVID-19.

That’s the view of Jean-Laurent Casanova, a geneticist at the Rockefeller University in New York City. He co-leads a consortium called the COVID Human Genetic Effort, which in September 2020 reported7 spotting mutations in people with severe COVID-19 that disable genes involved in a potent antiviral response, called type 1 interferon immunity. (One of the genes in which they found mutations, IFNAR2, which codes for a subunit of an interferon receptor, has also been flagged by multiple GWAS.) The mutations identified by Casanova’s team were rare, but in a follow-up study8, the researchers found that 10% of people with life-threatening COVID-19 produced antibodies that inactivate type 1 interferons — mimicking the effects of the gene mutations. Casanova says his team looked for them only after they identified the genetic mutations, underscoring the power of his approach to point to new lines of research. “Essentially what we’ve cracked is a mechanism of critical COVID-19 pneumonia,” he says.

Rare mutations with profound consequences are “a great torch to use” to uncover disease mechanisms, says Akiko Iwasaki, an immunologist at Yale University in New Haven, Connecticut, whose team is studying the role of ‘autoantibodies’, which attack the body’s own immune defences, in severe COVID-19. The effects of common variants identified in GWAS might be subtler, she adds, but the unbiased way in which they are identified means that the hits can give credence to insights from other disciplines, such as immunology. “It’s explaining some of the things we’re seeing,” she says. “I love that aspect of it.”

Richards is part of a team that is trying to replicate Casanova’s genetic finding, without success so far. He and his colleagues found that mutations in 13 type-1 interferon genes were no more common in nearly 2,000 people with COVID-19 than in controls not known to have been infected9, echoing the conclusions of an analysis led by researchers at the biotechnology firm Regeneron in Tarrytown, New York, who looked at protein-coding genes in more than half a million UK Biobank participants10. This doesn’t mean that the type 1 interferon pathways are not important, Richards says, and he agrees that the autoantibody connection looks promising.

Alessandra Renieri, a geneticist at the University of Siena, Italy, and an early member of the HGI, says that GWAS findings need to be integrated with links to rare variants and other forms of genetic diversity if researchers are to fully understand COVID-19 susceptibility, and to come up with treatments. She is part of a team that has applied for permission from Italian regulators to test therapies based on genetic findings.

For instance, the team wants to test an adjuvant (which awakens the immune system) in people with rare mutations that disable a virus-detecting gene called TLR7, which might be connected to severe COVID-1911. It also wants to test whether the hormone testosterone might be able to prevent life-threatening COVID-19 in men with a common variation in a gene that encodes a receptor for the hormone, after finding a link between severe COVID-19 and gene variants associated with reduced levels of testosterone circulating in the blood12.

The success of such trials should not be the only metric by which to judge the fruits of genetic studies into COVID-19, say researchers. Other biologists are drawing on the genetic studies to help make sense of their own experiments on the virus. And puzzling associations such as the chromosome 3 link could reveal important insights that help in treating COVID-19 — and whatever disease is caused by the next new coronavirus.

Each new genetic finding is like a piece of a puzzle, Renieri says. “Several pieces are coming together. I’m sure that the picture will be much more clear in the very near future.”

[ds4techofficial]

Coronavirus live updates | PM Modi's mother Hiraba gets vaccinated

Coronavirus live updates | PM Modi’s mother Hiraba gets vaccinated

Maharashtra, Tamil Nadu, Punjab, Madhya Pradesh, Delhi, Gujarat, Karnataka and Haryana continue to display an upward trajectory in daily new cases, the Union Health Ministry hsa said.   You can track coronavirus cases, deaths and testing rates at the national and State levels here. A list of State Helpline numbers is available as well. Here are the latest updates: Gujarat PM Modi’s nonagenarian…