Publication date: Jun 20, 2025
Virus infections pose a continuous threat to human health and can result in millions of deaths per year. SARS-CoV-2 infection has been linked to the high-affinity high-density lipoprotein (HDL) receptor scavenger receptor class B, type 1 (SR-B1). Mechanisms by which SR-B1 supports SARS-CoV-2 infection and replication, as well as the breadth of viruses that exploit this receptor, are incompletely defined. In evaluating the role of SR-B1 in the biology of infection with SARS-CoV-2, influenza A virus, and vesicular stomatitis virus, we show that SR-B1 chemical inhibition or knockout adversely affects infection for these viruses. Inhibiting SR-B1 results in lack of acidification in the endolysosomal compartment and entrapment of SARS-CoV-2 in endosomal-lysosomal vesicles. These findings together indicate that SR-B1, and possibly HDL, is critical for successful SARS-CoV-2 trafficking through a pH-dependent vesicular entry pathway. Our work provides insights into how SR-B1 can impact viral infection in human lung cells.
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| Concepts | Keywords |
|---|---|
| Knockout | Biochemistry |
| Lipoprotein | Biological sciences |
| Scavenger | Cell biology |
| Successful | Microbiology |
| Virus | Natural sciences |
| Viral microbiology | |
| Virology |
Semantics
| Type | Source | Name |
|---|---|---|
| disease | MESH | viral infection |
| disease | MESH | SARS-CoV-2 infection |
| pathway | REACTOME | SARS-CoV-2 Infection |
| disease | IDO | replication |
| disease | IDO | role |
| disease | MESH | infection |
| drug | DRUGBANK | Influenza A virus |
| disease | IDO | cell |