T cell signaling mechanisms that regulate HIV-1 infection

Immunol Res. 2001;23(2-3):167-77. doi: 10.1385/IR:23:2-3:167.

Abstract

The ability of human immunodeficiency virus type-1 (HIV-1) to establish a persistent infection is critically dependent on the cellular signals that regulate HIV-1 replication within target cells. The balance between numerous host factors that either enhance or suppress viral infection determines the clinical outcome. Perturbation of the steady-state level of viral replication can significantly influence the course and the speed at which the infection develops into clinical disease. Activation signals delivered to T cells by cytokines and antigen-presenting cells (APC), are key modulators of viral replication. Our laboratory seeks to decipher how HIV-1 exploits T cell signaling mechanisms and host factors that regulate viral replication. Elucidation of the molecular mechanisms by which cellular signals regulate the HIV-1 life cycle within target cells will significantly advance our understanding of host-virus interactions.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Antigen-Presenting Cells / immunology
  • CD4-Positive T-Lymphocytes / immunology
  • CD4-Positive T-Lymphocytes / virology
  • Cell Adhesion Molecules*
  • Cytokines / physiology
  • Dendritic Cells / immunology
  • Gene Products, nef / physiology
  • HIV Infections / immunology
  • HIV Infections / virology
  • HIV-1 / physiology*
  • Humans
  • Immunologic Memory
  • Lectins / physiology
  • Lectins, C-Type*
  • Lymphocyte Activation
  • Lymphoid Tissue / immunology
  • Receptors, Cell Surface / physiology
  • Signal Transduction / physiology*
  • T-Lymphocyte Subsets / physiology*
  • T-Lymphocyte Subsets / virology
  • Virus Replication / physiology*
  • nef Gene Products, Human Immunodeficiency Virus

Substances

  • Cell Adhesion Molecules
  • Cytokines
  • DC-specific ICAM-3 grabbing nonintegrin
  • Gene Products, nef
  • Lectins
  • Lectins, C-Type
  • Receptors, Cell Surface
  • nef Gene Products, Human Immunodeficiency Virus