All viruses accumulate genetic mutations, and most are insignificant. #SARSCoV2 is relatively stable as viruses go.
But every mutation is a roll of the dice, and with widespread transmission in the US, the virus has had abundant opportunities to change.šŸ¤¬
Some good news: None of these mutationsā€”including in spike proteinā€”appear to have made the #coronavirus deadlier.šŸ™šŸ¼

#COVID19 #SARSCoV2
āš ļøAs people gain immunityā€”either via infection or a #vaccineā€”the virus could be under selective pressure to evade the human immune response.

This could put us in the same situation as with flu, where we have to chase the virus and, as it mutates, tinker with our vaccine.
These new genetic data show the #SARSCoV2 virus arrived in Houston many timesā€”71% of the viruses that arrived initially were characterized by the D614G mutation originating in #China that scientists increasingly suspect may give the virus a biological advantage in spreading.šŸ˜·
By the 2nd wave of Houstonā€™s outbreak, the D614G variant leaped to 99.9% prevalenceā€”dominating the outbreak. The researchers found that people infected with this strain had higher loads of virus in their upper respiratory tracts, potentially making the virus more transmissible.šŸ˜·
An even larger study of the spread of the #coronavirus in the UK, based on ~25,000 genomes, also found evidence that this variant of the virus outdistances its competitors ā€œin a manner consistent with a selective advantage.ā€
These mutations occur randomly as #SARSCoV2 makes mistakes trying to copy its genomeā€”and every new infection gives a chance for more mutations, which in turn increases the chance that one of these mutations will be useful to the virus, just as D614G apparently already has been.
Bottom line: allowing #SARSCoV2 to spread like wildfire not only endangers human lives in the near term, but also gives the virus more shots on goal to mutate and become more contagious and/or deadly.šŸ˜·

#coronavirus #COVID19
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