Covid virus mutations may not increase transmissibility

London:  None of the mutations currently documented in the SARS-CoV-2, the virus responsible for the Covid-19 disease, appear to increase its transmissibility in humans, say researchers after analysing the virus genomes of over 46,000 people with Covid-19 from 99 countries.

“The number of SARS-CoV-2 genomes being generated for scientific research is staggering,” said study author Lucy van Dorp from the University College London in the UK.

“We realised early on in the pandemic that we needed new approaches to analyse enormous amounts of data in close to real-time to flag new mutations in the virus that could affect its transmission or symptom severity,” Dorp added.

The study, published in the journal Nature Communications, found that none of these mutations is making Covid-19 spread more rapidly.

The research team analysed a global dataset of virus genomes from 46,723 people with Covid-19, collected until the end of July 2020.

The researchers have so far identified 12,706 mutations in SARS-CoV-2, the virus causing Covid-19. For 398 of the mutations, there is a strong evidence that they have occurred repeatedly and independently.

Of those, the researchers honed in on 185 mutations which have occurred at least three times independently during the course of the pandemic.

To test if the mutations increase transmission of the virus, the researchers modelled the virus’s evolutionary tree.

The researchers found no evidence that any of the common mutations are increasing the virus’s transmissibility. Instead, they found most common mutations are neutral for the virus.

This includes one mutation in the virus spike protein called D614G, which has been widely reported as being a common mutation that may make the virus more transmissible.

The new evidence finds that this mutation is in fact not associated with significantly increasing transmission.

The researchers found that most of the common mutations appear to have been induced by the human immune system, rather than being the result of the virus adapting to its novel human host.

“This situation is in contrast with another analysis by the same team of what happened when SARS-CoV-2 later jumped from humans into farmed minks,” the study authors wrote.

(IANS)