B.1.617.2 Is More Efficient In Infecting Cells and Evading Control By Antibodies (Biology)

SARS-CoV-2 Delta variant, also known as lineage B.1.617.2, is a variant of lineage B.1.617 of SARS-CoV-2, the virus that causes COVID-19. It was first detected in India in late 2020. It has mutations in the gene encoding the SARS-CoV-2 spike protein causing the substitutions T478K, P681R and L452R, which are known to affect transmissibility of the virus as well as whether it can be neutralised by antibodies for previously circulating variants of the COVID-19 virus. It is rapidly spreading in other countries, so it is important to determine whether convalescent or vaccinated patients are protected against infection by this variant.

Now, Markus Hoffmann and colleagues answered this question using reporter particles pseudotyped with SARS-CoV-2 spike protein, which are suitable tools to study SARS-CoV-2 neutralization by antibodies.

At first they examined whether B.1.617.2 spike protein mediates robust entry into cell lines like Vero, 293 T, Caco-2 and Calu-3. They found that B.1.617.2 spike protein mediated entry into 293 T and Vero cells with same efficiency as WT spike protein. However, the entry of virus in Caco-2 (human, colon) and Calu-3 (human, lungs) cells is 1.5 and 2 fold more efficient than WT S, respectively.

They also found that, B.1.617.2 spike protein caused more and larger syncytia and quantification of cell-to-cell fusion revealed that fusion by B.1.617.2 spike protein was 2.5-fold more efficient as compared to WT-S. This could cause more tissue damage, and thus be more pathogenic, than previous variants or that viral spread via syncytium formation contributes to efficient inter- and intra-host spread of this variant.

In addition, it has been determined whether the entry of B.1.617.2 is suspectible to inhibition by recombinant antibodies with emergency use authorization for COVID-19 treatment. They showed that, B.1.617.2 evades control by antibodies induced upon infection and BNT162b2 vaccination, although with lower efficiency as compared to B.1.351.

“This finding would be compatible with increased vaccine breakthrough of B.1.617.2 but also suggests that BNT162b2 should still protect from B.1.617.2- induced COVID-19.”

Finally, they suggested that, treatment of infection with Bamlanivimab alone will be ineffective but they expect that Casirivimab, Imdevimab and Etesevimab will be beneficial to B.1.617.2 infected patients when administered early after infection.

Reference: Prerna Arora, Nadine Krueger, Amy Kempf, Inga Nehlmeier, Anzhalika Sidarovich, Luise Graichen, Anna-Sophie Moldenhauer, Martin S. Winkler, Sebastian Schulz, Hans-Martin Jaeck, Metodi V. Stankov, Georg M.N. Behrens, Stefan Poehlmann, Markus Hoffmann, “Increased lung cell entry of B.1.617.2 and evasion of antibodies induced by infection and BNT162b2 vaccination”, bioRxiv 2021.06.23.449568; doi: https://doi.org/10.1101/2021.06.23.449568

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