Abstract
BackgroundHIV-1 infected cells can establish new infections by crossing the vaginal epithelia and subsequently producing virus in a milieu that avoids the high microbicide concentrations of the vaginal lumen.FindingsTo address this problem, here, we report that pretreatment of HIV-infected peripheral blood mononuclear cells (PBMCs) with a 27 amino acid CD4-mimetic, M48U1, causes dramatic and prolonged reduction of infectious virus output, due to its induction of gp120 shedding.ConclusionsM48U1 may, therefore, be valuable for prophylaxis of mucosal HIV-1 transmission.
Highlights
HIV-1 infected cells can establish new infections by crossing the vaginal epithelia and subsequently producing virus in a milieu that avoids the high microbicide concentrations of the vaginal lumen
Receptive transmission at the vaginal mucosa is thought to be primarily caused by cell-free virus (CFV) [1], it may involve transfer of HIV-infected leucocytes present in semen [2,3]
The observation that CFV infection via the vaginal mucosa requires a ~103-106 higher virus dose [4] than is needed to establish infection by the intravenous route suggests that the healthy epithelium of the female genital tract is a robust barrier to HIV transmission
Summary
HIV-1 infected cells can establish new infections by crossing the vaginal epithelia and subsequently producing virus in a milieu that avoids the high microbicide concentrations of the vaginal lumen. Pretreatment with most ARVs did not inhibit virus production by infected cells as compared to the untreated control cultures (Figure 1B).
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