Abstract
Results Following HIV infection of SVGA reporter cells, very limited infection was detected. Further, no receptor or coreceptors except CXCR4 were present on astrocytes. To see further if viral replication is blocked in astrocytes, we infected PFA or SVGA cells with VSV pseudotyped NL4-3. High levels of p24 and robust LTR-GFP or LTR-gagGFP activation were seen. VSV-HIV infected reporter cells never lost green fluorescence and green cells were negative despite of continuous low Tat and Rev production. To rule out If Tat and Rev expression were from circular unintegrated HIV-DNA, Alu PCR revealed integration of viral DNA. Further, Tat or TNF-a reactivated the latent HIV in astrocytes and the latent HIV-SVGA cells upon co-culture transmitted the infection to Jurkat cells.
Highlights
In the brain, HIV infects microglia and macrophages productively while astrocytes are infected limitedly
Insufficient Tat Production Leads to Latent HIV Infection in
We investigated regulation of HIV infection in astrocytes
Summary
HIV infects microglia and macrophages productively while astrocytes are infected limitedly. Insufficient Tat Production Leads to Latent HIV Infection in Ashok Chauhan*‡, Suzanne Gartner, Nicole Benoit and Avi Nath Address: Department of Neurology, Johns Hopkins University, Baltimore, MD 21287
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