Endocytosis of human immunodeficiency virus 1 (HIV-1) in astrocytes: A fiery path to its destination. (January 2015)

• Record Type: Journal Article
• Authors: Chauhan, Ashok; Khandkar, Mehrab
• Is Part Of: Microbial pathogenesis. Volume 78(2015)
• Page Start: 1
• Page End: 6
• Publication Date: 2015-01
• Subjects: HIV-1 brain -- HIV-1 persistence -- Lysosomotropic drugs -- Chloroquine -- Proteasome inhibitors -- LSP1 -- Rab -- Rev -- Tat; Pathogenic microorganisms -- Periodicals; Pathology, Molecular -- Periodicals; Communicable Diseases -- microbiology -- Periodicals; Communicable Diseases -- parasitology -- Periodicals; Micro-organismes pathogènes -- Périodiques; Pathologie moléculaire -- Périodiques; Electronic journals; 616.9041
• DOI: 10.1016/j.micpath.2014.11.003
• Languages: English
• ISSNs: 0882-4010

Abstract

Abstract: Despite successful suppression of peripheral HIV-1 infection by combination antiretroviral therapy, immune activation by residual virus in the brain leads to HIV-associated neurocognitive disorders (HAND). In the brain, several types of cells, including microglia, perivascular macrophage, and astrocytes have been reported to be infected by HIV-1. Astrocytes, the most abundant cells in the brain, maintain homeostasis. The general consensus on HIV-1 infection in astrocytes is that it produces unproductive viral infection. HIV-1 enters astrocytes by pH-dependent endocytosis, leading to degradation of the virus in endosomes, but barely succeeds in infection. Here, we have discussed endocytosis-mediated HIV-1 entry and viral programming in astrocytes. Highlights: HIV-1 infection in astrocytes is impeded at the viral entry level. Astrocytes adsorb HIV-1 particles and release them within 10 days. HIV-1 infects astrocytes minimally by pH-dependent endocytosis. Inhibiting endosomal acidification or increasing endosomal pH by lysosomotropic agents, bolstered both M- and T-tropic HIV-1.