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Our lives have been turned upside down for a few months since the emergence of the new coronavirus, SARS-CoV-2. At the time of writing, the pandemic has According to the WHO, the World Health Organization, has killed more than 1.4 million people and infected more than 61 million people around the world. In Belgium, the death toll exceeded 16,000 a few days ago.
We now know that 80% of Covid-19 cases will not develop a severe form of the disease, although it may last and be more painful than the flu, they will stay at home. For the rest, 10-15% of infected people will need to be hospitalized and need oxygen. The extreme cases remain, less than 5%. These severe cases will be admitted to the ICU, intubated, and will require the help of a ventilator.
For months, studies on SARS-CoV-2 continued to better understand this new virus. In this article, we take stock of the state of knowledge, but also of the uncertainties surrounding this virus.
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Come back
If SARS-CoV-2 probably appeared before December 30, it was only on that date that it was reported globally via a network that specializes in this type of alert. The content of the message read: Pneumonia of unknown cause. The possibility that it was viral pneumonia had already been mentioned. We’ll be back …
The virus
Very soon, the genetic sequence of the virus was available. This allowed us to make comparisons with viruses we already knew and to classify them among coronaviruses. It was then quickly that we realized this newcomer was close to SARS-CoV, discovered in southeastern China in November 2002 and which a few months later infected more than 8,000 people, including 800 deaths.
The knowledge produced on SARS-CoV was initially used as a reference for the virus that occupied us for a few months, namely the SARS-CoV-2 and Covid-19 disease. Emmanuel André, microbiologist: “if, for example, how does the virus interact with the human body, through which receptors? Very quickly it was suggested, as with SARS, that these famous ACE2 receptors were the gateway to human cells for this new virus.“.
Over time, new knowledge showed that there were still subtle differences. Until recently, a team of scientists from Bristol found that this novel coronavirus could also bind to a second receptor, neuropilin-1.. This causes SARS-CoV-2 not only to develop differently, but also to cause a slightly different pathology.
“The real discoveries took time, but it was because we were able to study previous and similar viruses that we were able to move forward relatively quickly.“, comments the microbiologist. These years”of peace“as he says, between the appearance of new viruses, allow them to be studied and therefore allow, on the basis of similarities, to propose clues (vaccines, antivirals, etc.) at the time of the arrival of a new virus.
The peculiarity of SARS-CoV-2
There are therefore differences between these viruses. For Emmanuel André, the most important difference that has allowed the virus to make its niche in the human species is that, without forgetting the severe forms of the disease that we encounter every day in hospitals, in most cases it causes few or no symptoms. This feature allows the virus to spread strongly and rapidly within the population.
Also, and to make matters worse, infected people can infect others before the first symptoms appear and therefore continue their social life without realizing that they contaminate other citizens. “That, if we put ourselves in the place of a virus, it is a very important advantage to be able to spread quickly“.
If we compare, for example, the current SARS-CoV-2 with MERS-CoV, another coronavirus, the latter has a higher mortality that requires us to take precautions, protect ourselves, treat ourselves and therefore avoid contact with others. For the virus, this feature is a disadvantage.
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Has the virus mutated?
Above all, viruses like to multiply. But these copies aren’t perfect, there are always flaws in their genome. On the contrary, human cells have a control system that allows them to verify that the copy is identical, which protects us, for example, from too early aging or from forms of cancer.
“Viruses that have a much smaller genome and arsenal of proteins are unable to perform this check.“, Emmanuel André tells us about it. “And so, they make a copy, if it works, so much the better, if it doesn’t work, the virus is not viable and that’s okay, there will be more …“.
Conclusion, as viruses tolerate imperfect copies, there will naturally be accumulations of mutations in the genome. Some mutations sometimes go unnoticed, the virus will die or the change will have no impact.
The question behind these genetic mutations in the virus is whether they can ultimately reduce the effectiveness of different vaccines. Since the virus is no longer the same, will the vaccine still be effective? For Emmanuel André the question is legitimate, but it says: “what you should know is that the virus doesn’t have much chance of changing itself. If it changes too much, it will no longer be viable […] the vast majority of mutations will mean that it will rather lose in virulence and thus be at its disadvantage“.
In theory, a mutation that would make the virus more pathogenic is always possible, but the microbiologist continues: “this is probably what happened before the virus arrived in humans. At that point he had mutations that were useful to him in infecting humans, but now that he is very comfortable in his environment, there is little chance that the mutants will develop and be more pathogenic for him. humanity“.
At this stage, it would appear that current mutants do not have a sensitivity that varies from the immunity developed by a vaccine. However, the risk of the virus mutating and making the vaccine less effective exists, even if it is minimal. This implies the creation of a system for monitoring the evolution of genomes in the world in order to prevent this type of scenario. This would not involve reviewing everything, but the vaccine would have to be adapted.
►►► Also read : Coronavirus vaccine race: eleven candidates in all are in the final phase of testing, what are the differences
Finally, remember that the more we let the virus circulate and multiply significantly, the greater the risk it will find a mutation to its advantage. For Emmanuel André: “it is not because we have a vaccine in perspective that circulating the virus becomes a more acceptable strategy “.
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Note that the flu virus we know best is a little bit special and has the ability to mutate and change every year. This explains why the vaccine varies from year to year.
A seasonal virus?
We talked about it a lot after the first block. Is SARS CoV-2 a seasonal virus? We can observe that there are seasonal peaks. “The virus arrived at our house in the winter and when the sunny days arrived, although we were a little less careful, it took a while to start over“, analyzes the specialist. And in fact at the end of the summer the epidemic resumed with more vigor in Europe”.It is not a virus that we will see purely On / Off like some viruses that we do not see in the summer, but there is a seasonal trend that seems to be taking shape“.
The second part of this article, Covid-19 disease, will be published this Sunday 6 December 2020: Coronavirus: in a year, what we know about Covid-19 disease
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