Although much is still unknown, what we know about this new variant tells us important things about the virus: it can adapt to become more easily transmitted and may be more difficult to neutralize, and possibly surpass the vaccine. a small measure.
So far, SARS-CoV-2 has mutated at a fairly constant rate, with only one or two variations per month. Some variations have allowed scientists to pause, sometimes mutant to become more transmissible and other mutant to be more effective in preventing detection by our immune system. But with this new variant, called B.1.1.7, the virus has acquired 17 mutations while changing virus proteins, according to the Centers for Disease Control and Prevention, which affects four different viral proteins: the ear protein, ORF1ab, Orf8 and protein N, the major nucleocapsid.
While the large number of mutations in one variant is worrisome, what is perhaps most worrying is how the mutations, taken together, could change the way the virus works. One of the mutations, N501Y, increases the intensity of spike protein binding to the human ACE2 receptor, which can make it easier for the virus to take root in infected people. This mutation is likely that this new variant, first isolated in the UK in late September, now accounts for more than 60% of new infections in and around London.
A second mutation in the spike protein, 69-70del, removes two amino acids, the removal of which can allow the virus to evade some immune responses and, combined with another mutation, can make it more transmissible. The 69-70 mutation has been found in other varieties of strains, including the mink strain in Denmark, and appears to occur when patients carry the virus for several months under immune pressure, not necessarily from the immune system itself. patient, but from treatments such as convalescent plasma that pumps antibodies into the patient’s system.
A third mutation, P681H, occurs in what is known as the spike protein cleavage site, which is an area known to affect how easily the virus can enter and kill cells. Changes in this part of the virus could increase its ability to cause disease and lethality, although there is still no evidence to show that this new variant is more dangerous to humans. This mutation alone is enough to be disturbing. The fact that it is combined in this variant variety with another mutation in the Orf8 protein that can also increase pathogenicity, is cause for alarm.
Mutations that affect the other two proteins, ORF1ab and N protein, are also suspected to allow the virus to reproduce more quickly and evade the immune system, although much more research is needed to see how each of these 17 mutations affect how the virus works. Still, we know enough to make some assumptions.
First, SARS-CoV-2 knows how to adapt and adapt quickly, just like the flu virus. Therefore, we must be prepared for the possibility that the virus will be with us in the long run. Like a flu vaccine, a Covid-19 vaccine may not be a one-size-fits-all affair. We already know from a recent study published in the New England Journal of Medicine that the half-life of neutralizing antibodies to at least one vaccine, the Modern Vaccine, decreases relatively rapidly over a three-month period in which they respond more vigorously and shorter. in those who have a less vigorous response. Although the study was small, it is questionable whether a vaccine taken today will remain effective 12 months, 18 months or more in the future. B.1.1.7 tells us something new: not only can immunity be wiped out, but the potency of the vaccine itself can change if the virus changes. This is not to say that modern medicine cannot keep up with an evolving Covid-19 virus, as is the case with the flu. But it may not be as simple or as easy as many have hoped.
Second, with the 69-70del mutation we may encounter a medical paradox. In an effort to save the lives of immunocompromised people who were infected with the virus, providers sometimes administered several rounds of antibody treatments to their patients. In some cases, patients would recover after a round of treatment to get sick again and require another dose. Even in a single patient, immune suppression over a period of weeks and sometimes months provides the virus with a multitude of opportunities to learn our best defenses and mutate to be more effective in circumventing our immune system. Although the administration of antibody treatments can save a human life, a UK study hypothesized that it could also facilitate the creation of new strains of the virus.
Finally, the variant suggests that we should immediately begin planning the next generation of Covid vaccines to respond more effectively to a changing virus. You should wait for the authorized vaccines to be tested against the new variant. Companies have expressed confidence that their vaccine could be protected, and BioNTech has noted that their vaccine could be altered to combat the new variant.
However, it is worth studying more alternative vaccine targets that could be more effective in protecting the population against virus variants. Right now, most developing vaccines target the peak protein. This includes Moderna, Novovax and Johnson & Johnson vaccines, as well as adenovirus-based vaccines such as AstraZeneca. These vaccines may work against the current version of the virus, but if we want to stay ahead of the spread of the disease, we need to expand the goals of vaccines to include other proteins such as ORF1ab, Orf8 and N proteins or the protein ORF3b, which others have studied. Other countries have developed vaccines with more traditional methods, using inactivated whole virus. This type of vaccine or other vaccines targeting several proteins at once may be the best approach to move forward.
I often compare viruses to the machines that encode the code, continually running the numbers until they find a new way to exploit any ecological niche they inhabit: billions of copies of a virus each changing and adapting to each new challenge. Sometimes we come across a virus that learns to break down our defenses faster than we can rebuild them. I’m afraid SARS-CoV-2 may be one of them.