A new study has found that the new Covid-19 variant (501Y.V2) can evade neutralisation by first-wave anti-SARS-CoV-2 antibodies and potentially re-infect Covid-19 convalescent individuals.

The study, published in the preprint server bioRxiv, stated that 501Y.V2 is characterised by several mutations and has the propensity to escape antibody neutralisation.

The researchers noted in their study that this will cause widespread transmission. This transmissibility is linked to the inevitable increase in infection rates and death toll.

In this study, the researchers used simulation methods to investigate different mutations (E484K, K417N, and N501Y) at the spike receptor-binding domain (S RBD-ACE2) interface in the rapidly spreading South African variant 501Y.V2.

ACE2 are the receptor cells that SARS-CoV-2 uses to bind itself and make entry into host cells.

The study reported a greater affinity of South African strain for ACE2 in comparison to E484, as well as the greater probability of modified conformation when compared to the original structure.

This may actually represent mechanisms by which the new 501Y.V2 viral variant was able to replace original SARS-CoV-2 strains.

This improved affinity is a likely culprit for the more rapid spread of this variant due to greater transmissibility.

The researchers stated: "We believe the MD simulation approach used here similarly represents a tool to be used in the arsenal against the continuing pandemic, as it provides insight into the likelihood mutations alone or in combination may have effects that lessen the efficacy of existing therapies or vaccines."

"We suggest vaccines whose efficacies are largely dependent upon humoral responses to the S antigen only are inherently limited by the emergence of novel strains and dependent upon frequent re-design," they added.

Researchers mentioned that a vaccine that evokes a vigorous T-cell response is much less subject to changes due to accruing mutations and, thus, provides a better and more efficient approach to protection against this disease.

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