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me viruses naturally mutate, as specified by researchers at COVID-19 Genomics UK (COG-UK), a British organization dedicated to the analysis and sequencing of genome of the SARS-CoV-2 coronavirusTherefore, it is not surprising that the pathogen responsible for the pandemic that we are experiencing. There are thousands variants SARS-CoV-2 arose from these mutationsProfessor Lucy van Dorp, Professor of Microbial Genomics at the University of California, Los Angeles, noted in an article published in The Conversation magazine, however, in most cases they differ from each other by a small number of definitive mutations. This means that I stumps in circulation – at least five of which in Italy – have a genomic diversity limited and do not affect the fundamental characteristics of the coronavirus. However, in September the so-called “English variant” was identified B.1.1.7 characterized by 17 contemporary mutations (14 amino acids and 3 deletions), an “unprecedented” situation according to the authors of the study “Preliminary genomic characterization of an emerging SARS-CoV-2 lineage in the UK defined by a new set of mutations from peak “, which could be linked to an increase transmissibility 70 percent. Mutations can also make the virus more or less aggressive or even capable of evade a vaccineThat’s why mutated variants are in the sights of experts. But how does a virus mutate?
To better understand this biological mechanism, let’s take a step back starting from the structural characteristics of the new coronavirus. SARS-CoV-2 is a pathogen of the coronavirus subfamily (Orthocoronavirinae) characterized by a Genomic RNA composed of 30 thousand bases or “letters”. Each virion has a mean diameter of one hundred nanometers and its beating heart is represented by a very long sequence of thousands of letters. Mutations, in simple terms, are changes that occur in the organization / arrangement of these letters, groups of which refer to certain geni, which in turn codes for viral proteins. One of the key viral proteins of the coronavirus is protein S OR Spike, what the pathogen explodes as biological selection join ACE2-2 receiver of human cells, break the cell wall, pour the viral RNA inside to start the process replication causing infection.
The replication mechanism itself is the reason for determining the mutations. The virus must constantly replicate copies of itself to infect new cells and, as Professor Steve Wylie of Murdoch University explains, it exploits a enzyme called polymerase. Think of polymerase as a viral RNA “copier”. When the printing process occurs, the mechanism can jam, lead to errors that determine the substitution of one letter for another, or cancel it. The resulting mutated virus is often not significantly different from the original “wild” one, but the natural selection which may make it more or less suitable for the host it infects, or perhaps more effective for a new host. Not all viruses that circulate in others animals are capable of infecting humans, this is because key (such as coronavirus protein S) and door’s lock (receptors on human cells) do not match. But mutations can cause them to line up after millions of years of selection and replication, thus allowing the infamous leak (the jump of species). It is thanks to a favorable mutation that the SARS-CoV-2 coronavirus managed to jump from bats to man, directly or indirectly through an intermediate host, probably a pangolin.
Mutations continue to occur constantly, and as far as SARS-CoV-2 is concerned, as the (COG-UK) researchers explained in a press release, it accumulates 1-2 mutations per month as it replicates in infected people. Therefore, the genomes of the thousands of variants now circulating “differ by about 20 points from the first genomes sequenced in China in January,” specifies the authoritative scientific journal Science, noting however that “there are also many variants with fewer modifications” . The English variant is peculiar precisely because of the number of mutations accumulated at the same time, eight of which are located right in the protein S gene.It is not surprising that new variants continue to emerge in the future, as long as the coronavirus can replicate. in humans. The hope is that it can be killed by vaccines before it can produce mutations capable of doing so. resistant, to which we will have to respond with new preparations, a bit like every year, against influenza viruses, known for their remarkable mutant capacity.
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