Transcriptional Reprogramming during Effector-to-Memory Transition Renders CD4+ T Cells Permissive for Latent HIV-1 Infection

Immunity. 2017 Oct 17;47(4):766-775.e3. doi: 10.1016/j.immuni.2017.09.014.

Abstract

The latent reservoir for HIV-1 in resting memory CD4+ T cells is the major barrier to curing HIV-1 infection. Studies of HIV-1 latency have focused on regulation of viral gene expression in cells in which latent infection is established. However, it remains unclear how infection initially becomes latent. Here we described a unique set of properties of CD4+ T cells undergoing effector-to-memory transition including temporary upregulation of CCR5 expression and rapid downregulation of cellular gene transcription. These cells allowed completion of steps in the HIV-1 life cycle through integration but suppressed HIV-1 gene transcription, thus allowing the establishment of latency. CD4+ T cells in this stage were substantially more permissive for HIV-1 latent infection than other CD4+ T cells. Establishment of latent HIV-1 infection in CD4+ T could be inhibited by viral-specific CD8+ T cells, a result with implications for elimination of latent HIV-1 infection by T cell-based vaccines.

Publication types

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

MeSH terms

  • CD4-Positive T-Lymphocytes / immunology*
  • CD4-Positive T-Lymphocytes / metabolism
  • CD4-Positive T-Lymphocytes / virology
  • Cells, Cultured
  • Cellular Reprogramming / genetics
  • Cellular Reprogramming / immunology*
  • Cytokines / genetics
  • Cytokines / immunology
  • Female
  • Flow Cytometry
  • Gene Expression Profiling / methods
  • HIV-1 / immunology*
  • HIV-1 / physiology
  • Host-Pathogen Interactions / immunology
  • Humans
  • Immunologic Memory / genetics
  • Immunologic Memory / immunology*
  • Lymphocyte Activation / genetics
  • Lymphocyte Activation / immunology
  • Male
  • Reverse Transcriptase Polymerase Chain Reaction
  • T-Lymphocytes, Cytotoxic / immunology
  • T-Lymphocytes, Cytotoxic / metabolism
  • Transcription, Genetic*
  • Virus Latency / immunology
  • Virus Replication / immunology

Substances

  • Cytokines