HIV-1 hijacks HGF/c-MET signaling to promote viral entry and replication in primary CD4(+) T cells.

HIV-1 hijacks HGF/c-MET signaling to promote viral entry and replication in primary CD4(+) T cells, with c-MET disruption reducing infection markers by affecting receptor expression.

• Why it matters: Understanding host pathways exploited by HIV-1 is crucial for developing new therapeutic strategies, especially those targeting viral entry and replication mechanisms.
• What they did: The study used genetic knockout, knockdown, and pharmacological inhibition of c-MET in primary CD4(+) T cells, combined with RNA sequencing, flow cytometry, and infection assays, to investigate c-MET's role.
• The result: Disruption of c-MET decreased cell-surface CD4 and CXCR4, limiting viral entry, and attenuated activation of NF-κB, STAT1/3, and MAPK pathways, highlighting c-MET as a potential therapeutic target.