"This N501Y mutation provides a much higher efficiency of binding, which in turn makes the virus more infectious," said Victor Padilla-Sanchez, a research scientist at The Catholic University of America
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A team of researchers has examined why the UK and South African variants of SARS-CoV-2, the virus that causes Covid-19, are more infectious and, in many cases, more deadly. The study indicated that the UK variant, also known as B.1.1.7, has many mutations in the spike glycoprotein, but most important is one mutation, N501Y, in the receptor binding domain that interacts with the ACE2 receptor.
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"This N501Y mutation provides a much higher efficiency of binding, which in turn makes the virus more infectious," said Victor Padilla-Sanchez, a research scientist at The Catholic University of America. The UK variant was first detected in September 2020, and is now causing 98 per cent of all Covid-19 cases in the UK. The World Health Organization (WHO) said the UK variant is one of several variants of concern along with others that have emerged in South Africa and Brazil. The South Africa variant emerged in October 2020, and has more important changes in the spike protein, making it more dangerous than the UK variant.
According to the researchers, it involves a key mutation -- called E484K -- that helps the virus evade antibodies and parts of the immune system that can fight coronavirus based on experience from prior infection or a vaccine. Since the variant escapes immunity the body will not be able to fight the virus, the team said. All three variants have undergone changes to their spike protein -- the part of the virus which attaches to human cells. As a result, they are better at infecting cells and spreading them.
In the study, published in the journal Research Ideas and Outcomes, the team presented a computational analysis of the structure of the spike glycoprotein bound to the ACE2 receptor where the mutations have been introduced. "I've been analysing a recently published structure of the SARS-CoV-2 spike bound to the ACE2 receptor and found why the new variants are more transmissible," Padilla-Sanchez said.
"These findings have been obtained using the University of California - San Francisco Chimera software and molecular dynamics simulations using the Frontera supercomputer of the Texas Advanced Computing Center (TACC)," Padilla-Sanchez added. The researchers also performed structural analysis, which studied the virus's crystal structure; and molecular dynamics to obtain these findings.
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