Answers are grounded in this paper and cite their sources.
HIV infection modulates the surface expression of Tim-3, but the molecular determinants remain poorly understood. Here, we show that HIV-1 Vpu downregulates Tim-3 from the surface of infected primary CD4 + T cells through its transmembrane domain and alters its subcellular localization. Tim-3 blockade increases HIV-1 replication, suggesting a potential negative role of this protein in viral spread that is counteracted by Vpu.
No takes yet. Share an insight, caveat, or question.
Prévost et al. (2020) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: