Although many things are 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 be more difficult to neutralize and may be able to overcome the vaccine to a small extent. .
So far, SARS-CoV-2 has moved at a fairly constant rate, with only one or two variations per month. Some variations have given scientists a break, sometimes moving to become more transmissible and other times moving to become more effective in avoiding detection by our immune system. But with this new variant, called B.1.1.7, the virus has simultaneously acquired 17 mutations that modify the virus’s proteins, according to the Centers for Disease Control and Prevention, which affects four different viral proteins: spike protein, ORF1ab, Orf8 and N, major nucleocapsid.
While the large number of mutations in a variant is worrisome, what is probably more worrying is how the mutations, taken together, could change the way the virus works. One of the mutations, N501Y, increases how closely the spike protein binds to the human ACE2 receptor, which can make it easier for the virus to take root in infected people. This mutation is probably why this new variant, first isolated in the UK at the end of September, now accounts for more than 60% of new infections in and around London.
A second mutation in the spike protein, 69-70del, eliminates two amino acids, the removal of which can allow the virus to evade immune responses and, combined with another mutation, can make it more transmissible. The 69-70del mutation has been found in other variants 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 patient’s immune system, but from treatments such as plasma. convalescent pumping antibodies into the patient’s system.
A third mutation, P681H, occurs in what is called the spike protein cleavage site, which is an area known to affect how easily the virus can enter and destroy cells. Changes in this part of the virus could increase its ability to cause disease – and lethality – although there is still no evidence that this new variant is more dangerous to humans. This mutation alone is enough to be unsettling. The fact that it is combined in this strain variant with another mutation of the Orf8 protein, which can also increase pathogenicity, is really a cause for alarm.
Mutations that affect the other two proteins – ORF1ab and protein N – are also suspected to allow the virus to replicate faster and evade the immune system, although much more research is needed to see how each of these 17 mutations affect how the virus works. However, we know enough to make a few assumptions.
First of all, 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 deal. 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 of the vaccines, the Moderna vaccine, decreases relatively quickly over a three-month period in those who respond most vigorously. shorter to those with a less vigorous response. Although the study was small, it calls into question whether a vaccine given today will actually remain 12 months, 18 months or more in the future. B.1.1.7 tells us something new – not only can immunity be faded, but the potency of the vaccine itself can change if the virus changes. This does not mean 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 easy as many have hoped.
Second, with the 69-70del mutation we may face a medical paradox. In an effort to save the lives of immunocompromised individuals who have been infected with the virus, providers have sometimes given several rounds of antibody treatments to their patients. In some cases, patients would recover after one round of treatment only to become ill again and require another dose. Even in a single patient, suppressing immunity over a period of weeks and sometimes months gives the virus a multitude of opportunities to learn the best defenses and move to become more effective at bypassing our immune system. While the administration of antibody treatments can save a human life, a study in the UK has hypothesized that it could also facilitate the creation of new strains of the virus.
Finally, the option suggests that we need to start planning the next generation of Covid vaccines immediately to respond more effectively to a changing virus. It should give some hope that authorized vaccines are already being tested against the new variant. The companies expressed confidence that their vaccine could protect against it, with BioNTech noting that its vaccine could be modified to combat the new variant.
However, it is worth further studying the alternative vaccine targets that could prove more effective in protecting the population against virus variants. At this time, most developing vaccines target the spike protein. This includes Moderna, Novovax and Johnson & Johnson vaccines, as well as adenovirus-based vaccines such as AstraZeneca. These vaccines may work against today’s version of the virus, but if we want to stay ahead of the spread of the disease, we need to expand the targets for vaccines to include other proteins such as ORF1ab, Orf8 and N or ORF3b, which others have studied. Other countries have developed vaccines with more traditional methods, using fully inactivated virus. This type of vaccine, or other vaccines that target multiple proteins at the same time, may be the best approach to move forward.
They often compare viruses to code-coding machines, constantly running numbers until they find a new way to exploit any ecological niche they live in – trillions of copies of a single virus, each changing and adapting to each new challenge. Sometimes we face a virus that teaches us how to break through our defenses faster than we can rebuild them. I’m afraid SARS-CoV-2 may be one of them.