The D614G mutation can make SARS-CoV-2 more contagious



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According to a new study, the SARS-CoV-2 virus is accumulating genetic mutations, including one called D614G that may have made it more contagious.

SARS-CoV-2 particle next to an RNA strand, all orange on a dark orange to black gradient background

The researchers sequenced the genomes of SARS-CoV-2 strains taken from 5,085 COVID-19 patients in the Houston Metro, Texas, USA, and observed that the virus that causes COVID-19 is accumulating various genetic mutations. One of the study’s coauthors, Ilya Finkelstein, associate professor of molecular biosciences at the University of Texas at Austin (UT-Austin), explained that their study shows that “the virus is mutating due to a combination of neutral drift – which simply means random genetic changes that do not help or damage the virus and the pressure on our immune system. “

According to the paper, during the first wave of COVID-19 cases, 71 percent of the SARS-CoV-2 particles identified in patients in Houston had the D614G mutation. However, in the second wave of the outbreak during the summer, this variant had a prevalence of 99.9%. The researchers say this finding mirrors a trend seen around the world; A study published in July based on over 28,000 genomic sequences found that variants carrying the D614G mutation became the globally dominant form of SARS-CoV-2 in about a month.

But why has this strain become dominant and does the D614G mutation confer an advantage?

The researchers suggest the mutation could make the strain more contagious, as a study of more than 25,000 genomic sequences from the UK found that viruses with the D614G mutation tended to transmit slightly faster than those without it.

Researchers said natural selection would favor strains that are more easily transmitted; however, not all scientists are convinced and some suggest that the D614G mutation may have been more common in the first viruses to arrive in Europe and North America, essentially giving them an advantage over other strains, what they call ‘founder effects’.

The team also reported that the SARS-CoV-2 Spike (S) protein, which the virus uses to infect cells, continues to accumulate mutations of unknown significance. The team, made up of scientists from Houston Methodist Hospital, UT-Austin and elsewhere, also showed that one of the mutations allows protein S to evade neutralizing antibodies produced in response to viral infections. This mutation may allow SARS-CoV-2 to escape the immune system as well, so the researchers said it’s good that the mutation is rare and doesn’t appear to make the disease more severe for infected patients. According to Finkelstein, the team did not identify viruses that have learned to evade first-generation vaccines and therapeutic antibody formulations.

Scientists have noted a total of 285 mutations in thousands of infections, although most do not appear to have a significant effect on disease severity. Ongoing studies are continuing to examine the third wave of COVID-19 patients and characterize how the virus is adapting to the neutralizing antibodies produced by our immune system.

The article was published in mBIO.

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