Our life has been turned upside down for a few months by the emergence of the new coronavirus, SARS-CoV-2. At the time of writing, the pandemic had According to the World Health Organization, The World Health Organization, has killed more than 1.4 million people and infected more than 61 million people worldwide. In Belgium, the number of deaths exceeded the 16,000 mark a few days ago.
We now know that 80% of Covid-19 cases will not develop a serious form of the disease, although it can last and be more painful than the flu, they will stay at home. For the rest, 10 to 15% of infected people will have to be hospitalized and need oxygen. The extreme cases remain, less than 5%. These serious cases will be hospitalized in intensive care, incubated and require ventilator assistance.
For months, studies around SARS-CoV-2 have followed suit to better understand this new virus. In this article, we consider the state of knowledge, but also the uncertainty surrounding this virus.
If SARS-CoV-2 had apparently appeared before December 30, it was only reported on that date globally through a network specializing in this type of alert. Read contents of message: unknown cause pneumonia. The possibility of viral pneumonia has already been mentioned. We will come back …
Very early on, the genetic sequence of the virus became available. This made it possible to make comparisons with the viruses we already knew and distribute it among the coronaviruses. So we soon realized that this newcomer was close to the SARS-CoV, discovered in southeast China in November 2002 and which a few months later infected more than 8,000 people, 800 died.
The information generated on SARS-CoV was initially used as a reference for the virus that has occupied us for a few months, namely SARS-CoV-2 and Covid-19 disease. Emmanuel André, microbiologist: “whether, for example, how does the virus interact with the human body, through which receptors? Very quickly, it was suggested that, as with SARS, these famous ACE2 receptors were the gateway into human cells for this new virus.“.
Over time, new information showed that there are still subtle differences. Until recently, a team of scientists from Bristol discovered that this new coronavirus could also bind to a second receptor, Neuropilin-1. This causes SARS-CoV-2 to not only develop differently, but also cause a slightly different pathology.
“The real discoveries took time, but that was because we were able to study previous viruses and we were probably able to progress relatively quickly“, says the microbiologist. All these years”of peace“as he says, between the emergence of new viruses, allow them to be studied and then allow, on the basis of similarities, to offer leads (vaccines, antivirals, etc.) at the point of arrival of a new virus.
Specificity of SARS-CoV-2
So there are differences between these viruses. For Emmanuel André, the most important difference that has allowed the virus to make its way into the human species is that, not forgetting the serious forms of the disease that we encounter every day in hospitals, in most cases it is’ n causes few or no symptoms. This feature allows the virus to spread strongly and rapidly within the population.
Furthermore, and to make matters worse, infected people may infect others before the first symptoms appear and thus continue their social life without realizing that they are contaminating other citizens. “So if we replace ourselves with a virus, it’s 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 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.
Has the virus been mutated?
Above all, viruses like to multiply. But these copies are not perfect, there are always defects in their genome. Conversely, human cells have a control system that allows them to check that the copy is identical, which protects us, for example, from premature aging or from cancer types.
“Viruses with a much smaller genome and an arsenal of proteins cannot carry out this check.“, Emmanuel André tells us. “And so, they make a copy, if it works, so much better, if not, the virus is not viable and that’s fine, there will be more …“.
Conclusion, because viruses tolerate imperfect copies, there will naturally be mutations in the genome. Sometimes some mutations go unnoticed, the virus will either die or the switch will have no effect.
The question behind these genetic mutations in the virus is whether they can ultimately reduce the effectiveness of different vaccines. As the virus is no longer identical, will the vaccine still be effective? For Emmanuel André, the question is valid, but he says: “what you should know is that the virus has few possibilities to change itself. If it changes too much, it will no longer be viable […] the overwhelming majority of mutations will mean that it will instead lose in virulence and therefore be at a disadvantage“.
Theoretically, a mutation that would make the virus more pathogenic is always possible, but the microbiologist continues: “this is probably what happened before the virus reached humans. At that time he had mutations that had the benefit of infecting humans, but now that he is very good in his environment, there is little chance of mutants developing and more pathogenic to him. mankind“.
At this time, current mutants appear not to have a sensitivity that varies from the vaccine-developed immunity. However, the risk of the virus rolling out and making the vaccine less effective still exists even if it is very small. This includes setting up a system to monitor the evolution of genomes worldwide to prevent this kind of scenario. This would not mean reviewing everything, but the vaccine would have to be modified.
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Finally, remember that the more we allow the virus to circulate and multiply significantly, the greater the risk of finding a mutation to its advantage. For Emmanuel André: “Not because we have a vaccine in hopes that letting the virus circulate becomes a more acceptable strategy “.
Note that the flu virus we know better is a bit special and has this ability to roll and change every year. This explains why the vaccine varies from year to year.
We talked a lot about it after the first lockdown. Is SARS CoV-2 a seasonal virus? We can observe that there are seasonal peaks. “The virus arrived in our home in winter and when sunny days arrived, despite being a little less careful, it took a while to re-start“, analyzes the expert. And indeed in late summer, the epidemic resumed with more vigor in Europe.”It’s not a virus that we see as On / Off just like some viruses we don’t see in summer, but a seasonal trend that seems to be emerging“.
The second part of this article, the Covid-19 disease, will be published this Sunday, December 6, 2020: Coronavirus: early this year, what we know about the Covid-19 disease