London, May 8 (SocialNews.XYZ) Double-mutant variant of severe acute respiratory syndrome SARS-CoV-2 -- B.1.617 -- that has emerged in India, entered certain types of lung and intestine cells with slightly increased efficiency compared with the original wild-type strain, say researchers.
The researchers, including Markus Hoffmann from German Primate Center, also reported that the entry of B.1.617 into the lung and intestinal cells was blocked following treatment with soluble angiotensin-converting enzyme 2 (ACE2) or the serine protease inhibitor Camostat.
However, this host cell entry was not blocked by the monoclonal antibody Bamlanivimab, which has received emergency use authorisation (EUA) as a Covid-19 treatment.
Finally, B.1.617 also partially evaded neutralisation by the antibodies induced through natural infection or immunisation with the Pfizer-BioNTech BNT162b2 vaccine, a study that appeared in the pre-print repository medRxiv, suggested.
The researcher said that antibody evasion by B.1.617 may contribute to the rapid spread of this variant.
The sharp rise in Covid-19 cases and deaths in India over recent weeks is thought to be caused by the novel variant B.1.617, which harbours eight mutations in the spike protein.
These include the RBD mutations L452R and E484Q, which are known to modulate antibody-mediated neutralisation.
However, the researchers said it is not currently known whether B.1.617 resists this antibody-mediated neutralization.
To test whether B.1.617 is more adept at entering cells, the researchers infected eight cell lines with pseudotyped virus particles expressing spike protein from the original wild-type virus, the B.1.617 variant, or the B.1.351 variant.
Of the eight cell lines tested, the spikes of B.1.617 and B.1351 mediated entry into Calu-3 lung cells and Caco-2 colon cells with slightly increased efficiency, compared with the original strain.
Collectively, the study reveals that antibody evasion by B.1.617 may contribute to the rapid spread of this variant, the team noted.
Source: IANS
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