A study of the mutations of COVID-19 show one particularly problematic strain that delivers a higher viral load, making the virus more contagious than before, The Washington Post reported.
The higher viral load contributed to the rapid spread in the second wave, but the Houston-based researchers noted the mutations do not make the virus deadlier or change clinical outcomes, per the report.
All viruses develop mutations, but most are insignificant, according to researchers studying the 5,000 genetic sequences of the coronavirus. But, this one strain is mutating like the flu, which would mean the vaccines would have to "chase" it and evolve as well, according to experts.
The report noted 99% of the Houston second wave samples contained the mutation. It changed the structure of the "spike protein" that might have caused the massive spread of the strain, per the Post.
"We have given this virus a lot of chances," study author James Musser of Houston Methodist Hospital told the Post. "There is a huge population size out there right now."
According to Global Initiative on Sharing All Influenza Data:
"A mutation affecting the spike protein changed amino acid 614 from 'D' (aspartic acid) to 'G' (glycine). Research suggests that this small change — which affects three identical amino acid chains — might enhance the virus' transmissibility."
"Wearing masks, washing our hands, all those things are barriers to transmissibility, or contagion, but as the virus becomes more contagious it statistically is better at getting around those barriers," National Institute of Allergy and Infectious Diseases senior adviser to NIAID Director Dr. Anthony Fauci, David Morens, told the Post.
"Although we don't know yet, it is well within the realm of possibility that this coronavirus, when our population-level immunity gets high enough, this coronavirus will find a way to get around our immunity. If that happened, we'd be in the same situation as with flu. We'll have to chase the virus and, as it mutates, we'll have to tinker with our vaccine."
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