| Autor: |
Ghorpade, Anuja, Nukuna, Adeline, Che, MyHanh, Haggerty, Sheryl, Persidsky, Yuri, Carter, Eboni, Carhart, Leeroy, Shafer, Laura, Gendelman, Howard E. |
| Zdroj: |
The Journal of Virology; April 1998, Vol. 72 Issue: 4 p3340-3350, 11p |
| Abstrakt: |
ABSTRACTProductive replication of human immunodeficiency virus type 1 (HIV-1) in brain macrophages and microglia is a critical component of viral neuropathogenesis. However, how virus-macrophage interactions lead to neurological disease remains incompletely understood. Possibly, a differential ability of virus to replicate in brain tissue macrophages versus macrophages in other tissues underlies HIV-1 neurovirulence. To these ends, we established systems for the isolation and propagation of pure populations of human microglia and then analyzed the viral life cycles of divergent HIV-1 strains in these cells and in cultured monocytes by using identical viral inocula and indicator systems. The HIV-1 isolates included those isolated from blood, lung tissue, cerebrospinal fluids (CSF), and brain tissues of infected subjects: HIV-1ADAand HIV-189.6(from peripheral blood mononuclear cells), HIV-1DJVand HIV-1JR-FL(from brain tissue), HIV-1SF162(from CSF), and HIV-1BAL(from lung tissue). The synthesis of viral nucleic acids and viral mRNA, cytopathicity, and release of progeny virions were assessed. A significant heterogeneity among macrophage-tropic isolates for infection of monocytes and microglia was demonstrated. Importantly, a complete analysis of the viral life cycle revealed no preferential differences in the abilities of the HIV-1 strains tested to replicate in microglia and/or monocytes. Macrophage tropism likely dictates the abilities of HIV-1 to invade, replicate, and incite disease within its microglial target cells. |
| Databáze: |
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