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Impact of HIV-1 Membrane Cholesterol on Cell-Independent Lytic Inactivation and Cellular Infectivity
Journal article   Open access   Peer reviewed

Impact of HIV-1 Membrane Cholesterol on Cell-Independent Lytic Inactivation and Cellular Infectivity

Ramalingam Venkat Kalyana Sundaram, Huiyuan Li, Lauren Bailey, Adel A Rashad, Rachna Aneja, Karl Weiss, James Huynh, Arangaserry Rosemary Bastian, Elisabeth Papazoglou, Cameron Abrams, …
Biochemistry (Easton), v 55(3), pp 447-458
26 Jan 2016
PMID: 26713837
url
https://doi.org/10.1021/acs.biochem.5b00936View
Published, Version of Record (VoR) Open

Abstract

HIV-1 - pathogenicity Peptides - chemistry Sulfhydryl Compounds - pharmacology HIV-1 - drug effects Triazoles - chemistry Humans Cholesterol - metabolism Membrane Fluidity HIV Envelope Protein gp120 - metabolism beta-Cyclodextrins - pharmacology Peptides - pharmacology Triazoles - pharmacology HIV-1 - physiology Cell Line, Tumor HIV Core Protein p24 - metabolism Membrane Lipids - metabolism Sulfhydryl Compounds - chemistry Thiazoles - chemistry Thiazoles - pharmacology
Peptide triazole thiols (PTTs) have been found previously to bind to HIV-1 Env spike gp120 and cause irreversible virus inactivation by shedding gp120 and lytically releasing luminal capsid protein p24. Since the virions remain visually intact, lysis appears to occur via limited membrane destabilization. To better understand the PTT-triggered membrane transformation involved, we investigated the role of envelope cholesterol on p24 release by measuring the effect of cholesterol depletion using methyl beta-cyclodextrin (MβCD). An unexpected bell-shaped response of PTT-induced lysis to [MβCD] was observed, involving lysis enhancement at low [MβCD] vs loss of function at high [MβCD]. The impact of cholesterol depletion on PTT-induced lysis was reversed by adding exogenous cholesterol and other sterols that support membrane rafts, while sterols that do not support rafts induced only limited reversal. Cholesterol depletion appears to cause a reduced energy barrier to lysis as judged by decreased temperature dependence with MβCD. Enhancement/replenishment responses to [MβCD] also were observed for HIV-1 infectivity, consistent with a similar energy barrier effect in the membrane transformation of virus cell fusion. Overall, the results argue that cholesterol in the HIV-1 envelope is important for balancing virus stability and membrane transformation, and that partial depletion, while increasing infectivity, also makes the virus more fragile. The results also reinforce the argument that the lytic inactivation and infectivity processes are mechanistically related and that membrane transformations occurring during lysis can provide an experimental window to investigate membrane and protein factors important for HIV-1 cell entry.

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Collaboration types
Domestic collaboration
Web of Science research areas
Biochemistry & Molecular Biology
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