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

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Peptide triazole thiols (PTTs) inactivate HIV-1 by releasing capsid protein p24. Cholesterol depletion affects this lysis in a bell-shaped manner, impacting virus stability and infectivity.

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Area of Science:

  • Virology
  • Biochemistry
  • Membrane Biophysics

Background:

  • Peptide triazole thiols (PTTs) inactivate HIV-1 by targeting the Env spike gp120.
  • This inactivation involves shedding gp120 and releasing capsid protein p24 through lysis.
  • The mechanism of PTT-induced lysis, particularly the role of the viral envelope, requires further investigation.

Purpose of the Study:

  • To investigate the role of cholesterol in the HIV-1 envelope on PTT-induced lysis.
  • To understand how cholesterol depletion affects the release of capsid protein p24.
  • To explore the relationship between envelope cholesterol, virus stability, and infectivity.

Main Methods:

  • Cholesterol depletion from HIV-1 virions using methyl beta-cyclodextrin (MβCD).
  • Measurement of p24 release to quantify lysis.
  • Assessment of HIV-1 infectivity under varying MβCD concentrations.
  • Reversal experiments using exogenous cholesterol and other sterols.

Main Results:

  • A bell-shaped dose-response curve was observed for MβCD concentration affecting PTT-induced lysis.
  • Low MβCD enhanced lysis, while high MβCD inhibited it.
  • Cholesterol depletion reduced the energy barrier for lysis and increased HIV-1 infectivity.
  • Exogenous cholesterol and raft-supporting sterols reversed the effects of depletion.

Conclusions:

  • HIV-1 envelope cholesterol is crucial for balancing virus stability and membrane transformation.
  • Partial cholesterol depletion increases infectivity but also viral fragility.
  • Lytic inactivation and infectivity are mechanistically linked, offering insights into HIV-1 entry.