Benzotriazoles Reactivate Latent HIV-1 through Inactivation of STAT5 SUMOylation

Cell Rep. 2017 Jan 31;18(5):1324-1334. doi: 10.1016/j.celrep.2017.01.022.

Abstract

The presence of latent HIV-1 in infected individuals represents a major barrier preventing viral eradication. For that reason, reactivation of latent viruses in the presence of antiretroviral regimens has been proposed as a therapeutic strategy to achieve remission. We screened for small molecules and identified several benzotriazole derivatives with the ability to reactivate latent HIV-1. In the presence of IL-2, benzotriazoles reactivated and reduced the latent reservoir in primary cells, and, remarkably, viral reactivation was achieved without inducing cell proliferation, T cell activation, or cytokine release. Mechanistic studies showed that benzotriazoles block SUMOylation of phosphorylated STAT5, increasing STAT5's activity and occupancy of the HIV-1 LTR. Our results identify benzotriazoles as latency reversing agents and STAT5 signaling and SUMOylation as targets for HIV-1 eradication strategies. These compounds represent a different direction in the search for "shock and kill" therapies.

Keywords: HIV-1 latency; HIV-1 reservoir; STAT5; SUMOylation; benzotriazoles; latency reversing agent; shock and kill.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Cell Proliferation / drug effects
  • HIV Infections / metabolism*
  • HIV Infections / virology
  • HIV-1 / drug effects*
  • Humans
  • Interleukin-2 / metabolism
  • Lymphocyte Activation / drug effects
  • STAT5 Transcription Factor / metabolism*
  • Small Molecule Libraries / pharmacology
  • Sumoylation / drug effects*
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / metabolism
  • Triazoles / pharmacology*
  • Virus Activation / drug effects*
  • Virus Latency / drug effects*

Substances

  • Interleukin-2
  • STAT5 Transcription Factor
  • Small Molecule Libraries
  • Triazoles
  • benzotriazole