Incorporation of podoplanin into HIV released from HEK-293T cells, but not PBMC, is required for efficient binding to the attachment factor CLEC-2.

摘要: Background: Platelets are associated with HIV in the blood of infected individuals and might modulate viral dissemination, particularly if virus is directly transmitted into bloodstream. The C-type lectin DC-SIGN novel attachment factor CLEC-2 expressed by platelets facilitate transmission from to T-cells. Here, we studied molecular mechanisms behind CLEC-2-mediated HIV-1 transmission. Results: Binding studies soluble proteins indicated that CLEC-2, contrast DC-SIGN, does not recognize envelope protein, but a cellular on kidney-derived 293T cells. Subsequent analyses revealed mucin-like membranous glycoprotein podoplanin, ligand, was cells incorporated virions released these Knock-down podoplanin shRNA showed virion incorporation required for efficient CLEC-2-dependent interactions cell lines platelets. Flow cytometry no evidence expression viable T-cells peripheral mononuclear (PBMC). Podoplanin also detected However, apoptotic bystander cultures reacted anti-podoplanin antibodies, similar results were obtained upon induction apoptosis line PBMCs suggesting an unexpected link between expression. Despite absence detectable expression, produced PBMC Tcells manner, indicating express as yet unidentified ligand. Conclusions: Virion mediates derived cells, while different seems be responsible capture PBMC-derived viruses. Furthermore, connected apoptosis, finding deserves further investigation.