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Industrial-Scale Genome Sequencing-It’s Fascinating and Frightening to See the Evolution of SARS-CoV-2 | Quarterly Technology




March 23, 2021

Initial identification of SARS-CoV-2 and genomic sequencing, which is important for providing vaccine templates for it, also provided a new way to monitor pandemic progression. Viruses often make mistakes when copying the genome, which is an important step in reproduction. That is, the virus accumulates mutations very quickly. You can see the actual evolution by sequencing enough samples over time. During the first six months of the pandemic, this was a matter of academic interest and, not a little, a sign. Last fall, bad news that evolution students were afraid of began to appear in the data.

The first inking was a sample taken from a patient in Kent, a county in the southeastern part of England, on September 20th. When sequenced by the Covid-19 Genomics UK Consortium, it was found to be the largest such evolutionary surveillance effort in the world, with an unusually large number of mutations. Subsequent sequencing showed that this new mutant was spreading rapidly. By November, I was responsible for a quarter of the new cases in London. By December it had risen to almost 60%. By February, it accounted for more than 90% of infections in some UK regions, and also according to Hezi Levi, head of the Israeli Ministry of Health. What the British started was, as expected, spread all over the world. As is known, by mid-March 25-30% of new American cases were thought to have been caused by B.1.1.7.

Due to its rapid spread, B.1.1.7 became a variant of concern, even before evidence began to show that it was more likely to cause the disease than the original strain. Currently, two other related variants have been added. B.1.351 was first discovered in a South African sample taken in October, and P.1 began distribution in Brazil in November or December, but its presence is 4 from Brazil to Japan. It was first confirmed by a number of visitors when it was discovered in January. P.1 spreads as rapidly as B.1.1.7. It can overwhelm Brazil’s intensive care capacity. But that’s not the only unfortunate innovation. Like B.1.351, P.1 is the wrong foot antibody created to recognize the original version of SARS-CoV-2. It does not matter whether the antibody occurs naturally in the infected body, is produced in cell culture by a pharmaceutical company, or is the result of vaccination.

In all three cases, mutations are concentrated in the genes that explain peplomer. One mutation in that gene, N501Y, is common to all three. That wouldn’t be a coincidence. Rather, it suggests that this mutation helps the virus.

Spikes bind to proteins in human cells so that the virus can invade human cells. Therefore, that bit of binding is very important for its success and is the best possible target for the antibody. If evolution has a goal for it, they would say that it should bind better to the target, and the bit that binds should be more difficult for the antibody to neutralize. Mutations accumulated in the subspecies of interest seem to do just that. N501Y makes the binding tighter. E484K, also known as eek, reduces the effectiveness of the antibody. Originally a feature of P.1 and B.1.351, it is now found in both UK and US B.1.1.7 samples.

These variants are problematic for Eli Lilly and Regeneron, which provide antibodies as drugs against the virus. Both companies sell cocktails that contain two different antibodies. One of the release antibodies does not work against B.1.351. The other looks a bit like iffyas does one of Regenerons.

Antibodies are a niche concern. Even more worrisome is what the new variants mean for vaccination. Preliminary studies show that volunteers who participated in the Oxford / AstraZeneca vaccine trial are both slightly less effective and more uncertain, as are volunteers infected with previous variants, in terms of disease protection. This was despite the fact that these volunteer antibodies were less able to bind to B.1.1.7 particles than other viral particles. Vaccines stimulate much of the immune system, not just the bits that make antibodies.

The Novavax vaccine, which consists of cell-cultured peplomer and has not yet been approved, provides excellent protection against disease of B.1.1.7 and fair protection of B.1.351 (60%). The Johnson & Johnson vaccine is also effective against its mutants. Tests on how other vaccines deal with mutants of concern have not yet been published. However, all vaccine makers know that they need to show a spike in the immune system version that elicits a response that can handle the entire range of mutants. The mRNA and adenovirus companies have confirmed that new versions of the peplomer gene sequence can be loaded into the production system if needed. Novavax needs to redesign the cells used to generate that version of the spikes.

Not all changes are bad

It may need to be done on a regular basis to know when the vaccine needs to be renewed. With regard to influenza vaccines, other countries need to emulate the UK’s diligence in sequence monitoring. Currently, the UK sample dominates the sequence database of Gisaid, a Munich-based international partnership originally established to track influenza outbreaks (see graph). More careful testing in the United States has already picked up new variants. B.1.526, which appears to have taken off in New York at the end of last year, boasts both D253G, which has a similar effect to the eek mutation. A study by a group led by Jeremy Kamil of Louisiana State University, available as a preprint on February 14, identified seven variants of concern. Obviously of independent origin, most share a spike mutation called Q677P. This suggests that this is another change that is strongly supported by natural selection.

Discovering where variants have emerged and quickly assessing the additional risks they pose should be a central part of the fight against the virus. It could also be a way to monitor any outbreak of SARS-CoV-2. New pathogens often follow an evolutionary process, which reduces pathogenicity and thereby increases infectivity. I think some people may explain the origin of four relatively benign coronaviruses, which are generally known to cause the symptoms labeled as the common cold.

A study published in 2005 on the latest variant of one of these, OC43, suggests that the latest common ancestor lived around 1890. This is consistent with the pandemic historically known as the Russian flu. It was due to science. Therefore, it is believed that the real cause was the toxic ancestor of OC43. The idea that SARS-CoV-2 may proceed in the same way and eventually evolve into something less threatening than the common cold may sound like wishful thinking. But it is possible.

This article was published in the printed Technology Quarterly section under the heading “Know your enemy”.

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