New Variant Covid-19 VUI 202012/01

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Woodchopper
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Re: New Variant Covid-19 VUI 202012/01

Post by Woodchopper » Wed Mar 03, 2021 8:48 pm

Estimated transmissibility and impact of SARS-CoV-2 lineage B.1.1.7 in England
https://science.sciencemag.org/content/ ... g3055.full

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Re: New Variant Covid-19 VUI 202012/01

Post by Woodchopper » Thu Mar 04, 2021 5:57 pm

Resistance of SARS-CoV-2 variants to neutralization by monoclonal and serum-derived polyclonal antibodies
https://www.nature.com/articles/s41591-021-01294-w

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Re: New Variant Covid-19 VUI 202012/01

Post by Woodchopper » Sat Mar 06, 2021 10:25 am

Study from Denmark:

Infection with lineage B.1.1.7 was associated with an increased risk of hospitalisation compared with other lineages. This finding may have serious public health impact in countries with spread of B.1.1.7 and can support hospital preparedness and modelling of projected impact of the epidemic.
https://papers.ssrn.com/sol3/papers.cfm ... id=3792894

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Re: New Variant Covid-19 VUI 202012/01

Post by Woodchopper » Tue Mar 09, 2021 12:22 pm

Case fatality risk of the SARS-CoV-2 variant of concern B.1.1.7 in England
The B.1.1.7 variant of concern (VOC) is increasing in prevalence across Europe. Accurate estimation of disease severity associated with this VOC is critical for pandemic planning. We found increased risk of death for VOC compared with non-VOC cases in England (HR: 1.67 (95% CI: 1.34 - 2.09; P<.0001). Absolute risk of death by 28-days increased with age and comorbidities. VOC has potential to spread faster with higher mortality than the pandemic to date.
https://www.medrxiv.org/content/10.1101 ... 21252528v1

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Re: New Variant Covid-19 VUI 202012/01

Post by Woodchopper » Tue Mar 09, 2021 8:30 pm

Quantification of the spread of SARS-CoV-2 variant B.1.1.7 in Switzerland
https://www.medrxiv.org/content/10.1101 ... 21252520v1

Pretty much the same as in Britain

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Re: New Variant Covid-19 VUI 202012/01

Post by Woodchopper » Sat Mar 20, 2021 7:01 pm


The coronavirus variant first discovered in the United Kingdom may account for up to 30% of new COVID infections across the U.S., NIAID Director Anthony Fauci said during a White House briefing on the virus Friday.
https://www.axios.com/fauci-uk-variant- ... ae509.html

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Re: New Variant Covid-19 VUI 202012/01

Post by Woodchopper » Sat Mar 20, 2021 7:14 pm


Mutations at both the receptor-binding domain (RBD) and the amino (N)-terminal domain (NTD) of the SARS-CoV-2 Spike (S) glycoprotein can alter its antigenicity and promote immune escape. We identified that SARS-CoV-2 lineages circulating in Brazil with mutations of concern in the RBD independently acquired convergent deletions and insertions in the NTD of the S protein, which altered the NTD antigenic-supersite and other predicted epitopes at this region. These findings support that the ongoing widespread transmission of SARS-CoV-2 in Brazil is generating new viral lineages that might be more resistant to neutralization than parental variants of concern.
https://www.medrxiv.org/content/10.1101 ... 21253946v1

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Re: New Variant Covid-19 VUI 202012/01

Post by Woodchopper » Sun Apr 04, 2021 8:48 am


Increased mortality in community-tested cases of SARS-CoV-2 lineage B.1.1.7


SARS-CoV-2 lineage B.1.1.7, a variant first detected in the UK in September 20201, has spread to multiple countries worldwide. Several studies have established that B.1.1.7 is more transmissible than preexisting variants, but have not identified whether it leads to any change in disease severity2. Here we analyse a dataset linking 2,245,263 positive SARS-CoV-2 community tests and 17,452 COVID-19 deaths in England from 1 September 2020 to 14 February 2021. For 1,146,534 (51%) of these tests, the presence or absence of B.1.1.7 can be identified because of mutations in this lineage preventing PCR amplification of the spike gene target (S gene target failure, SGTF1). Based on 4,945 deaths with known SGTF status, we estimate that the hazard of death associated with SGTF is 55% (95% CI 39–72%) higher after adjustment for age, sex, ethnicity, deprivation, care home residence, local authority of residence and test date. This corresponds to the absolute risk of death for a 55–69-year-old male increasing from 0.6% to 0.9% (95% CI 0.8–1.0%) within 28 days after a positive test in the community. Correcting for misclassification of SGTF and missingness in SGTF status, we estimate a 61% (42–82%) higher hazard of death associated with B.1.1.7. Our analysis suggests that B.1.1.7 is not only more transmissible than preexisting SARS-CoV-2 variants, but may also cause more severe illness.
https://www.nature.com/articles/s41586-021-03426-1

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Re: New Variant Covid-19 VUI 202012/01

Post by Woodchopper » Mon Jun 07, 2021 7:54 pm


How the ‘Alpha’ Coronavirus Variant Became So Powerful

A new study suggests how the variant first identified in Britain hides from the human immune system. Its stealth may be part of its success.

[...]

Alpha has 23 mutations that set it apart from other coronaviruses. When the variant started to surge in Britain, researchers began inspecting these genetic tweaks to look for explanations as to why it was spreading faster than other variants.

[...]

scientists have focused on how Alpha affects the human immune response. Gregory Towers, a virologist at the University College London, and his colleagues grew coronaviruses in human lung cells, comparing Alpha-infected cells with those infected with earlier variants of the coronavirus.

They found that lung cells with Alpha made drastically less interferon, a protein that switches on a host of immune defenses. They also found that in the Alpha cells, the defensive genes normally switched on by interferon were quieter than in cells infected with other variants.

Somehow, the immune system’s most important alarm bells were barely ringing in the presence of the Alpha variant. “It’s making itself more invisible,” Dr. Towers said.

To investigate how Alpha achieved this invisibility, the researchers looked at how the coronavirus replicated inside of infected cells. They found that Alpha-infected cells make a lot of extra copies — some 80 times more than other versions of the virus — of a gene called Orf9b.

“It’s off the chart,” said Nevan Krogan, a molecular biologist at the University of California, San Francisco, and a co-author of the new study.

In previous research, Dr. Krogan and his colleagues had found that Orf9b makes a viral protein that locks onto a human protein called Tom70. And it just so happens that Tom70 is essential for a cell’s release of interferon in the face of an invading virus.

Putting all of the evidence together, Dr. Krogan and his colleagues argue that the Alpha variant carries a mutation that forces the production of a lot more Orf9b proteins. Those proteins swarm the human Tom70 proteins, dampening the production of interferon and a full immune response. The virus, protected from attack, has better odds of making copies of itself.

An infected cell can gradually remove the Orf9b proteins from its Tom70 molecules, however. By about 12 hours after infection, the alarm system starts coming back online. And because of that immune response, Dr. Towers said, “all hell breaks loose.”

Dr. Towers speculated that when the delayed immune response finally happens, people infected with Alpha have a more robust reaction than they would with other variants, coughing and shedding virus-laden mucus from not only their mouths, but also their noses — making Alpha even better at spreading.

[...]

Dr. Krogan’s team has also started similar experiments on other variants, including the variant first identified in South Africa, known as Beta, and the one first identified in India, known as Delta. The preliminary results surprised them.

Both Beta and Delta drive down interferon in infected cells. But there’s no sign that they do so by flooding the cells with Orf9b proteins. They may have independently evolved their own tricks for manipulating our immune system.

“They’re all turning down the immune response in different ways,” Dr. Krogan said.
https://www.nytimes.com/2021/06/07/heal ... riant.html

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