Almost immediately after the onset of the epidemic, researchers began to search for patterns of change among the tens of thousands of sequences in the viral genome of SARS-CoV-2. The research was made possible thanks to the willingness of researchers around the world to upload their data to a common database. The data is open source, which means that anyone with a computer can access and analyze the data.
The alert that a change in the genome of SARS-CoV-2 was underway appeared for the first time from researchers skilled in the art of deciphering the coded messages in the genome of HIV-1, the virus that causes AIDS. The ability to find meaning in over a billion bits of this information has been refined by decades of research into the constantly evolving genomes of HIV-1, which can make a difference in life or death in the way whose virus responds to antiviral drugs. Once you know the history of the genomes, you can choose which drugs to use to treat a specific strain of the virus.
Researchers studying the genome of SARS-CoV-2 first noticed that one mutation, known as D614G, dominated all the others. It first appeared in February as a rare variant in Europe, before spreading and surpassing other strains in Italy and other countries. The research team quickly identified a single change in the genome of the virus. The mutation affects the advanced protein on the outer surface of the virus, for which the coronavirus is named (the Latin word corona means "crown" or "halo"). The tip is of particular importance in the life of the virus, because it is the mechanism that allows the virus to recognize itself and attach itself to a host cell before infecting it. The original authors hypothesized that the change improves the ability of the virus to adhere tightly to the mucous membranes of the nose or eyes to begin the process of infection.
The original report was greeted with skepticism. Some have asked whether the dominance of this new strain was the result of an independent phenomenon. Since the researchers relied only on publicly available data and computer analyzes of the genome, they could not definitively conclude that their idea was the only reasonable explanation for the emergence of the new dominant strain.
Until now.
The Scripps Research Institute in Florida answered this question in an unrevised research manuscript released on Friday. The researchers used an elegant set of methods to show that a small mutation stabilized the peak protein, which usually detaches from the surface of the virus. "The mutation had the effect of greatly increasing the number of functional spikes on the viral surface," said lead author Hyeryun Choe. "The number - or density - of functional peaks on the virus is 4 to 5 times higher due to this mutation." Result: each mutant viral particle has an increased ability to infect target cells.
This study clearly shows that the virus is evolving. He also revealed that the mutation was almost 10 times more infectious in the laboratory than the other strains. With genomic analyzes showing that this strain has become the dominant strain, the results could explain why the new coronavirus has spread so widely in Europe, the United States and Latin America.
Does more transmissible mean that the strain is more deadly? Not that we can observe, for now. From the point of view of the virus and its ability to survive, it is better to allow those who have been infected to live and spread the virus than to die.
Is this the end of the evolution of SARS-CoV-2? Not far. Doctors in northeast China noted that patients in a new group of cases appear to be carrying the virus for a longer period of time and take longer to test negative. They also found that patients took longer to show symptoms after infection. The virus may be mutating to become more persistent as another way to survive, as those who carry the virus for a longer period of time are more likely to infect others. Understanding the biochemical basis of this change will be fascinating.
Last month, a pair of manuscripts examined variants in one of the SARS-CoV-2 proteins, specified by the orf3b gene, which suppresses part of our immune response to viral infections. A particular variant of orf3b does this more effectively than the original, which can give the virus more time to replicate in the absence of an effective immune response. A sicker patient can be the result.
Since this week, SARS-CoV-2 has infected more than 7.6 million people. This is remarkable for a virus that most likely started with the infection of a single person about six months ago. SARS-CoV-2 now has an additional seven million chances to adapt to its new human ecosystem, and it looks like the virus is doing a good job.
We know from our experience with many viruses like HIV-1 and the flu that we are not faced with a static enemy. The new coronavirus is changing as we struggle to control the pandemic. SARS-CoV-2 has already proven to be a formidable adversary. If our success today - although probably limited - is important, we must not lose sight of the long battle against microbes that awaits us.
