While much is still unknown, what we do know about this new variant tells us important things about the virus: It can adapt to become more transmittable and become more difficult to neutralize, and could potentially outsmart the vaccine for a small one. extent.
To date, SARS-CoV-2 has mutated fairly constantly, with only one or two variations per month. Some variations have given scientists a break, sometimes they mutate to become more transmissible and sometimes they mutate to become more effective in avoiding detection by our immune system. But with this new variant, called B.1.1.7, the virus has acquired 17 mutations all at once that alter the virus’s proteins, according to the Centers for Disease Control and Prevention, that affect four different viral proteins: the spike protein. , ORF1ab, Orf8 and the N protein, the major nucleocapsid.
While the sheer number of mutations in one variant is alarming, perhaps even more concerning is how the mutations, taken together, can alter the way the virus works. One of the mutations, N501Y, increases the extent to which the spike protein binds to the human ACE2 receptor, making it easier for the virus to take root in infected individuals. This mutation is likely why this new variant, first isolated in the UK in late September, is now responsible for more than 60% of new infections in and around London.
A second mutation of the spike protein, 69-70del, removes two amino acids, the removal of which allows the virus to evade certain immune responses and, in combination with another mutation, makes it more transmissible. The 69-70del mutation has been found in other variant strains – including the mink strain in Denmark – and appears to occur when patients carry the virus under immune pressure for several months, not necessarily from the patient’s own immune system, but from treatments such as restorative plasma that pumps antibodies into the patient’s system.
A third mutation, P681H, occurs in the so-called cleavage site of the spike protein, a region known to affect how easily the virus can enter and kill cells. Changes in this part of the virus could potentially increase its ability to cause disease – and its lethality – although there is no evidence yet that this new variant is more dangerous to humans. This mutation alone is enough to be troubling. The fact that it is combined in this variant with another mutation in the Orf8 protein that can also increase pathogenicity is a cause for concern.
The mutations that affect the two other proteins – ORF1ab and the N protein – are also thought to allow the virus to replicate more quickly and evade the immune system, although much more research is needed to see how each of these these 17 mutations affect how the virus works. Still, we know enough to make a few assumptions.
First, SARS-CoV-2 knows how to adapt and adapt quickly, just like the flu virus. We must therefore be prepared for the possibility that the virus will stay with us in the long term. Like a flu vaccine, a Covid-19 vaccine may not be a one-off affair. We already know from a recent study published in the New England Journal of Medicine that the half-life of the neutralizing antibodies of at least one of the vaccines, the Moderna vaccine, decreases relatively quickly over a three-month period in those who respond the most . powerful and shorter in those who build a less powerful response. Although the study was small, it begs the question of 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 fade, but the potency of the vaccine itself can shift as the virus changes. This is not to say that modern medicine cannot keep up with the evolving Covid-19 virus, as is the case with the flu. But it may not be as simple or as easy as many would have hoped.
Second, with the 69-70del mutation, we may be faced with a medical paradox. In an effort to save the lives of immunocompromised people infected with the virus, health care providers sometimes administered multiple rounds of antibody treatments to their patients. In some cases, patients recovered after one round of treatment only to become ill again and require a new dose. Even in a single patient, immune suppression over a period of weeks and sometimes months gives the virus a multitude of opportunities to learn and mutate our best defense mechanisms to become more effective at evading our immune systems. While administering antibody treatments can save one 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 start planning for the next generation of Covid vaccines to respond more effectively to an altering virus. It should give some hope that the approved vaccines are already being tested against the new variant. The companies have expressed confidence that their vaccine could protect against this, with BioNTech noting that the vaccine could be modified to combat the new variant.
Still, it is worthwhile to further study alternative vaccine targets that could prove more effective in protecting the population against virus variants. Currently, most vaccines in development target the spike protein. This includes the Moderna, Novovax and Johnson & Johnson vaccines, as well as adenovirus based vaccines such as those from AstraZeneca. These vaccines may work against the current version of the virus, but if we want to stay ahead of the spread of disease we need to expand the targets for vaccines to include other proteins such as the ORF1ab, Orf8 and N proteins or the ORF3b protein, that others have studied. Other countries have developed vaccines using more traditional methods using inactivated whole virus. This type of vaccine, or other vaccines that target multiple proteins at once, may be the best approach for moving forward.
I often compare viruses to code-cracking machines, going through the numbers continuously until they find a new way to exploit the ecological niche they inhabit – trillions of copies of a single virus that change and adapt to each new challenge. Sometimes we come across a virus that is learning how to crack our defenses faster than we can rebuild them. I am concerned that SARS-CoV-2 could be one of them.