Writing in Nature, a team led by Cambridge researchers report how they were able to observe SARS-CoV-2 mutating in the case of an immunocompromised patient treated with convalescent plasma. In particular, they saw the emergence of a key mutation also seen in the new variant that led to the UK being forced once again into strict lockdown, though there is no suggestion that the variant originated from this patient.
Using a synthetic version of the virus Spike protein created in the lab, the team showed that specific changes to its genetic code – the mutation seen in the B1.1.7 variant – made the virus twice as infectious on cells as the more common strain.
SARS-CoV-2, the virus that causes COVID-19, is a betacoronavirus. Its RNA – its genetic code – is comprised of a series of nucleotides (chemical structures represented by the letters A, C, G and U). As the virus replicates itself, this code can be mis-transcribed, leading to errors, known as mutations. Coronaviruses have a relatively modest mutation rate at around 23 nucleotide substitutions per year.
That is interesting for them to note the process. Does that mean every virus particle that cannot get access to a cell to replicate will mutate its spike until it can strike lucky. Like a key on a bunch of keys just keep trying until one clicks . It gains entry and then a whole cell full of virus copies armed with the new keý are releasedWhere do the T cells and B cells come in .?
From how I understand it. What happens is that you get infected and the T-cells memorise the virus and instruct the B-cells to manufacture antibodies against the virus, Killer T-cells destroy infected any cells against it and eventually stop the replication of and kill the virus.
But with a severe infection and a higher viral load, the infected cells replicate the virus and mutate to avoid the produced antibodies, it seems to be able detect that the original, newly produced virus particles are not working and replicating. The higher viral load gives the virus more chances of mutation and the odds of success to avoiding the antibodies increases, eventually becoming the more dominant strain. This is then transmitted to another person to infect them and onto spread further. The increased mortality probably comes from a more efficient entry into the host cells giving a higher viral load.
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