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Cell surface TMPRSS11E interacts with CD98 to mediate SARS-CoV2 efficient entry of M1 macrophage

ABSTRACT: SARS-CoV-2 caused the global COVID-19 outbreak. Monocyte/macrophage were also target cells of sars-cov-2. How SARS-CoV-2 invade monocyte/macrophage remain poorly understood. Here, we showed that in classically activated M1 macrophage, SARS-CoV-2 exhibited greater infectivity compared with M2. CD98 and its light chain subunits forms heteromeric amino acid transporters. Here, upregulated CD98 in M1 was identified as novel receptor for SARS-CoV-2 spike. Moreover, TMPRSS11E expressed in M1, a paralog of TMPRSS2, was revealed to participate in the cleavage of SARS-CoV-2 spike and facilitate virus induced-membrane fusion. More interestingly, the homotypic aggregation in THP1 stably expressing TMPRSS11E was observed; RNA-seq revealed that overexpressing TMPRSS11E altered expression of many cytoskeleton related genes. Immunoprecipitations showed that TMPRSS11E and other cell surface adhesion molecules CD98 or CD147 were physically associated. Previously, CD147 was also reported the receptor for SARS-CoV-2. These results indicated TMPRSS11E and partner receptors interacted to form complexes that increase virus entry.

ORGANISM(S): Homo sapiens

PROVIDER: GSE289384 | GEO | 2026/05/15

REPOSITORIES: GEO

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