We know about the new SARS strain that is shutting down the UK

A variant of the pandemic coronovirus, SARS-CoV-2, is now dominating the headlines and prompting precautionary travel restrictions worldwide. But scientists are still trying to get a grip on what can actually be done differently and what that might mean for a nearly one-year epidemic.

Researchers in the United Kingdom — where the variant was identified and are now spreading rapidly — suggested that it may be 70 percent more infectious than other SARS-CoV-2 strains, which on the eve of the year The fear increases as the disease progresses – the last holiday. But other researchers are now increasingly working to collect data on the interactions of variants with human cells and immune responses to see if those interactions are different from those observed by other SARS-COV-2 strains.

What we know

Although much is known about this version, dubbed B.1.1.7, there are some reassuring aspects. For one thing, it is normal for viruses to accumulate small genetic changes, such as those that have made new UK versions (more on that below). Many other variants have been identified during the epidemic, and no one has had any nightmares.

So far, there is no reason to think that things will change much with the new one. There is no evidence yet that B.1.1.7 causes isolated or more severe COVID-19 disease; It does not present to make COVID-19 treatments less effective. UK officials also suspect that the newly authorized vaccines will only work against the new version, although researchers are working in haste to confirm this.

Together, the information at hand should change slightly about recommended strategies to try to eject the B.1.1.7 pandemic, regardless of which version is wandering through a population. “The bottom line is that we need to suppress the transmission of all SARS-COV-2 viruses,” World Health Organization Director General Tedros Adnom Ghebayeus said in a press briefing on Monday.

It is also important to increase the transmission capacity in perspective. While the “up to 70 percent” figure is indeed worrisome, the actual jump in transmission rates is minor. In the UK, the presence of B.1.1.7 increased the reproductive number of the virus from just 0.4 to 1.1 to 1.5, according to Maria Van Kerkhov, WHO’s technical lead on the COVID-19 pandemic. That small increase means that the number of people infecting each infected person went from 1 person to 1.5 people on average. It is unclear whether this increase is due to something inherent about the virus, the behavior of infected people, or a combination of the two.

The increase of 0.4 is not good news, but it is also not dramatically worse, with WHO’s executive director of emergency programs Drs. Mike Ryan has mentioned. The reproduction number of 1.5 can be controlled, he said, and the reproduction number of the virus during this epidemic is much higher at many other times.

“[This] Just keep the bar up a bit, “Ryan said.” We are not talking about breeding numbers like measles, which is somewhere between 12 and 18, or mumps and chickenpox, between 10 and 12. We are talking about 1.5. Viruses may be slightly more efficient at transmission – when we are infecting so many people, the numbers can have a big impact. But that means the virus can be contained, the virus can be suppressed [using] Same interference, exactly the same behavior as before.

Emphasizing the last point, Van Kerkhov elaborated that there is no reason to think of a minor bump in transmission as the virus has changed how it spreads from one person to another – moving in the air or Spreading more easily on surfaces. “It’s a respiratory pathogen, so it spreads between me and you through these particles in the air,” Van Kerkhov explained. “What is happening mainly is that the virus spreads between people who are in close contact with each other. It’s still the same.”

something new

While the WHO emphasized the similarity between B.1.1.7 and other strains of SAR.1-CoV-2, the UK government is focusing on what’s new. This is where the strain was first identified, and most people infected with it are in Britain.

Ongoing surveillance work within the UK made the details of the new strain clear, where researchers sequentially sequenced the genomes of dozens of virus samples each month. Over the course of the epidemic, circulating strains of SARS-CoV-2 have generally picked up one or two mutations on average in a month, so this level of surveillance is sufficient to follow the origin and spread of new strains. But B.1.1.7, first seen in samples obtained at the end of September, was nothing like the gradual accumulation of changes we saw earlier. There were 17 differences between it and the closest known strain to overcome the B.1.1.7 branch on the coronovirus family tree.

It is a curiosity rather than a concern “on its own”. There was correlation to grab people’s attention. In response to the winter wave of infection across Europe, Britain had resumed a set of social sanctions aimed at bringing back the level of infection. And in most countries of the country, those sanctions were intended. But not in the south-east and east of Britain. And it was precisely in the region where B.1.1.7 stress level was the highest. In one county, B.1.1.7 accounted for more than 20 percent of all new infections by mid-December, and the number has since gone up.

This is not conclusive evidence that strain B.1.1.7 has any benefit. The COVID-19 epidemic has been marked by numerous “superspreader” events and social groups that flout public health measures. This combination can cause a rapid expansion of tensions that are propagating within these groups at opportune moments. But as of this weekend, B.1.1.7 accounted for around 60 per cent of new cases in London, prompting government officials there to claim that tensions could spread more quickly.

However, to ensure this, we have to engineer the mutations found in B.1.1.7 into a lab strain and then test its infectivity. Meanwhile, scientists have looked at mutations present in the new viral strain and speculated about which ones could potentially confer infectivity to it or alter the course of infection.

Old but in a new combination

While B.1.1.7 represents a new strain of coronavirus, we know a fair amount about coronovirus biology, allowing us to determine when mutations alter a critical region. And in some cases, mutations have been found individually in different strains that we have previously shown. Therefore it is possible to infer some things about the behavior of B.1.1.7.

Many of them contain spike proteins that reside on the surface of the coronavirus and help them latch a protein on the surface of cells. One of the mutations found in B.1.1.7 is specifically part of a spike that participates in this process and has been found to increase the relationship between viral and human proteins. Another mutation removes two amino acids from the spike protein; It is associated with a decreased immune response but is usually only found in combination with other mutations (as here).

Finally, another mutation is next to a site where the spike protein is cut into two smaller pieces, something that is required for its function. While the mutation is not characterized, its location is suggestive.

Another mutation found in B.1.1.7 completely eliminates a viral protein (called ORF8). A distinct mutation that harms this gene was found in Singapore in the first year, and it causes less severe symptoms in infected people. But due to Singapore’s successful control of the epidemic, there are no active infections with that strain, so we have no further data there.


There is also some suggestive information that can be gathered from the collection of mutations found in B.1.1.7 as a whole. The 17 mutations that characterize it alter the proteins encoded by 14 viruses; Only three make no changes. This is a very high percentage and is often a sign of evolutionary selection for certain changes.

The high rate of mutation that is required to produce B.1.1.7 in a relatively short period of time has also been observed previously in individuals with immune infections. In these individuals, the infection may take more than a month to resolve, and they are often given treatments that directly target the virus, such as convulsions and plasma. Thus, it is possible that at least some changes are seen here due to selective evolutionary pressures arising from these treatments. (The researchers behind this analysis note that this is a hypothesis, rather than a conclusion that we have reached.)

While all these differences are suggestive, it is important to emphasize that we have no firm evidence that any of them change the behavior of the virus. Therefore, while the data on its spread are dramatic, we are still not certain whether these mutations are a product, and their effect on the course of viral infection is largely a matter of speculation. Although we wait for biologists to catch up with the changes found in B.1.1.7, WHO’s advice remains simple: be extra sure to take measures that public health experts have been advising for months. Huh.

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