Chaitanya Kurhade

Nov 6, 2024 | digitalcommons.library.tmc.edu | Panke Qu |John Evans |Chaitanya Kurhade |Cong Zeng

AbstractThe rapid spread and strong immune evasion of the SARS-CoV-2 Omicron subvariants has raised serious concerns for the global COVID-19 pandemic. These new variants exhibit generally reduced fusogenicity and increased endosomal entry pathway utilization compared to the ancestral D614G variant, the underlying mechanisms of which remain elusive. Here, we show that the C-terminal S1 mutations of the BA.1.1 subvariant, H655Y and T547K, critically govern the low fusogenicity of Omicron.