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meIt was always predictable that the Sars-CoV-2 genome would mutate. After all, that’s what viruses and other microorganisms do. The Sars-CoV-2 genome accumulates about one or two mutations each month as it circulates. In fact, its rate of change is much lower than that of other viruses that we know of. For example, seasonal influenza mutates at such a rate that a new vaccine must be introduced each year.
Even so, over time, the virus population will accumulate a few mutations in different combinations. The surprising feature of the 1.1.7 Sars-CoV-2 lineage that we discovered here at the Covid-19 Genomics UK Consortium (now known to headlines as the “new variant”), is that its genome has a large number of mutations in comparison. with other lineages we have collected in the UK. He has a total of 23, which is what sets him apart.
Most mutations are not of concern because they do not result in a change in one of the amino acids that make up the proteins the virus is made of. When they do, that deserves serious attention, especially when the mutations (or deletions) occur in a region of the virus that could change the way it interacts with its human host. In particular, changes in the spike protein, which adorns the exterior of the virus and is the mechanism by which it adheres to and enters the host cell, where it can replicate, are of great interest.
What worries scientists about the 1.1.7 lineage is that, along with six mutations that don’t change any proteins, there are 17 (14 mutations and three deletions) that do. A preliminary genomic analysis of the 1.1.7 lineage shows that several of these mutations have been described before in other lineages and have been found to change the way the virus behaves. A mutation (called 501Y) has been shown to increase the strength with which the protein binds to a receptor on the surface of human cells. A second change (69-70del) has been identified in viruses that evolved to evade the natural immune response in some immunosuppressed patients. But nothing can be assumed about the new variant and what these mutations mean. We need more scientific evidence to understand how this particular version of the virus behaves compared to others.
This is what we must take into account: if the variant is transmitted more easily between people, if it causes a more (or less) serious disease and if it can evade the immune response of our body. There is currently no evidence that the 1.1.7 lineage causes more serious disease or that it bypasses the immune system. There is also no reason to think that vaccines that are being implemented or in development will be less effective against it. But what seems increasingly likely is that this lineage is more transmittable.
In the UK, the body considering new evidence on the virus is the New and Emerging Respiratory Virus Threat Advisory Group (Nervtag). The latest publicly available minutes show that Nervtag has “moderate confidence” that this new variant is substantially more transmissible. The data he examined included a genomic analysis showing that this particular lineage was growing around 70% faster. Furthermore, he found a correlation between a higher R-value and the detection of the new variant in the test samples. (The R-value, remember, is the number of people each person transmits it to. The higher it is, the more it spreads.) They also noted that the variant grew exponentially during a period in which national lockdown measures were implemented. There are still possible other explanations for this rapid spread, but the idea that this variant is more transmissible is plausible and seems increasingly likely. The laboratory studies that are now being done will answer this with certainty.
What this means in practical terms is that all of our efforts to prevent the spread – through hand washing, wearing masks, and social distancing – become even more important. There is nothing to suggest that the new bloodline is capable of eluding them in any way, as long as we do them correctly.
One question that may never be answered is where the new variant came from. The first place we detected it, looking back through virus samples, was Kent and London. But it is not clear if it really arose there. It’s worth remembering that the UK carries out far more Sars-CoV-2 sequences than many other countries, and the fact that we found it here may say more about that than its eventual origin. Interestingly, it has been suggested that the variant may have arisen in an immunosuppressed person who was chronically infected, with the virus capable of replicating and evolving in them over a long period of time. But, as always, more work is required to understand if this is really the case.
Looking ahead, we must review our systems to predict whether a given mutation could have health implications. In a recent mutation survey by our consortium, based on 126,219 genomes from positive samples, it was possible to identify 1,777 different amino acid-changing mutations in the spike protein gene.
The identification of concerned mutations is an imperfect process. There are tools available that model changes in viral structure and function for any given mutation, but this modeling must always be confirmed by evidence. Not only that, but the sheer number of mutations that need to be modeled is huge. For now, the way we identify mutations that could be important to human health is by tracking the rate of spread of the virus, carefully monitoring the severity of the disease, and having systems to alert us when the virus has been able to evade past immunity. . infection or vaccination. The new variant first came to light at the end of November, when Public Health England was looking at why infection rates in Kent weren’t declining despite national restrictions, and we tied this observation with genome data.
The history of the new variant shows how important genome sequencing is, but underscores the fact that only when genome data is linked to epidemiological and clinical information can they make a difference in disease control. Fortunately, unlike past epidemics, we can use this tool quickly and on an unprecedented scale. We should be grateful for that, because it’s safe to assume that this won’t be the last time it’s needed.
