{
  "id": 163706,
  "title": "HIV-1 Hijacks HGF/c-MET Signaling to Promote Viral Entry and Replication in Primary CD4⁺ T Cells",
  "url": "https://urgent.news/2026/08/04/hiv-1-hijacks-hgf-c-met-signaling-to-promote-viral-entry-and",
  "topic": "science",
  "section": "Science",
  "published": "2026-08-04T00:00:00.000Z",
  "source": {
    "name": "bioRxiv",
    "slug": "biorxiv",
    "url": "https://www.biorxiv.org/content/10.64898/2026.08.03.742552v1?rss=1"
  },
  "original_language": "en",
  "account": "A recent study has uncovered an unexpected role for the HGF/c-MET signaling pathway in the replication of HIV-1 within primary CD4+ T cells. The mesenchymal-epithelial transition factor (c-MET) is typically associated with regulating hepatocyte growth factor (HGF) signaling in cancer, but its involvement in HIV-1 infection had not been previously identified.\n\nThe researchers found that HIV-1 infection leads to an increase in c-MET transcripts and phosphorylation in primary CD4+ T cells. When c-MET was knocked out or inhibited pharmacologically in these cells, HIV-1 replication was significantly reduced, as evidenced by decreased levels of the viral protein Gag, lower viral production, and diminished infectivity.\n\nBy disrupting c-MET, the researchers observed a reduction in the expression of both CD4 and CXCR4, the coreceptors necessary for HIV-1 entry into CD4+ T cells. This suggested that c-MET plays a crucial role in maintaining these receptor availability, thereby facilitating viral entry.\n\nFurthermore, the study revealed that c-MET inhibition dampened the activation of key signaling pathways such as NF-{kappa}B, STAT1/3, and MAPK, which are essential for the expression of HIV-1 genes. This indicates that c-MET signaling not only modulates receptor availability but also influences the intracellular signaling necessary for viral gene expression.\n\nThese findings demonstrate that HIV-1 exploits the HGF/c-MET signaling pathway to orchestrate both the availability of viral entry receptors and the intracellular pathways required for viral replication in primary CD4+ T cells. The discovery highlights an essential role for HGF/c-MET signaling in HIV-1 infection of these cells and suggests that targeting this host factor could be a promising therapeutic strategy to combat HIV-1 infection.",
  "summary": "The mesenchymal-epithelial transition factor (c-MET) is a receptor tyrosine kinase best known for mediating hepatocyte growth factor (HGF) signaling in cancer, yet its role in HIV-1 infection remains undefined. Here we identify c-MET as a host factor that facilitates HIV-1 replication in CD4+ T cells by promoting viral entry. HIV-1 infection upregulates c-MET transcripts and phosphorylation in…",
  "key_points": [],
  "editors_take": null,
  "illustration": null,
  "coverage": {
    "outlets": 1,
    "also_reported_by": []
  },
  "ai_generated": true,
  "disclaimer": "Summaries, key points and the editor’s take are written by software from other outlets’ reporting and may contain errors — always check the linked original."
}