ArticlePloS one2025
Amino acid residues 655 and 969 in the spike protein of Omicron subvariant BA.1 control use of TMPRSS2 versus Cathepsin L dependent entry pathways and cell tropism.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The spike (S) protein of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is activated by the host cell proteases cathepsin L or TMPRSS2. The ancestral virus circulating in Wuhan in 2020 and early variants mainly use TMPRSS2 for entry into Calu-3 lung cells while the Omicron subvariant BA.1 and most subsequently circulating Omicron subvariants employ both cathepsin L and TMPRSS2 for Calu-3 cell entry. Here, we investigated which amino acid residues in the S protein of the Omicron subvariant BA.1 control protease choice. We show that Y655 promotes S protein cleavage and cathepsin L-dependent entry while H655 jointly with N969 promotes TMPRSS2-dependent entry. These results define molecular signatures of SARS-CoV-2 protease choice and lung cell infection.
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