Science

Mutation of Covid-19 detrimental to certain T cell immune responses: Study

Prashasti Awasthi Mumbai | Updated on February 05, 2021

A new study on coronavirus mutation has reported that its B.1.1.7 variant (UK variant), with its characteristic N501Y mutation, impacts CD4 T cell responses significantly.

CD4 T cell responses support the immune response by the robust generation of cytokines and chemokines that, in turn, fight pathogens and prevent infection.

The study, published in the preprint server bioRxiv* server, noted that over 70 per cent of convalescent Covid-19 patients have CD4 T cells reactive to SARS-CoV-2; their activity is directly proportional to specific IgG antibody titers.

However, these cells are also reactive to the virus in 40-60 per cent of unexposed individuals. This indicates that the seasonal “common cold” coronaviruses activates a subset of CD4 T cells that later recognise the common antigens on SARS-CoV-2.

The researchers said these mutations seem to promote binding between the spike and ACE2, and the enhanced binding at this site perhaps explains the rapid rise to dominance of this strain.

The findings also suggest that the presence of some other specific mutations such as E484K may amplify the effect of the N501Y mutation on these characteristics of the virus, making them highly virulent.

Another explanation provided by the researchers revealed that the mutation affects the adaptive immune response, which involves B and T cells. The MHC system coordinates the key molecule in this intricate dance of immune cells and antigens. But to activate the B and T cell responses, RBD has to make contact with the ACE2 receptor that would necessarily have to bind MHC-II molecules.

However, the N501Y mutant has less binding affinity due to which the body is unable to activate T and B cells.

This could promote the more rapid spread of all such variants by its favourable effect on spike-ACE2 binding and its unfavourable impact on MHC-II binding for the majority of alleles.

Published on February 05, 2021

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