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Inducible-costimulator-mediated suppression of human immunodeficiency virus type 1 replication in CD4(+) T

Xin Zhou1, Makoto Kubo, Hironori Nishitsuji

  • 1Department of Immunotherapeutics, Graduate School, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.

Virology
|July 13, 2004
PubMed

Insights

Signaling through inducible costimulator (ICOS) molecules suppresses human immunodeficiency virus type 1 (HIV-1) replication in immune cells. This suggests ICOS ligands may offer a new strategy for controlling HIV-1 infection.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Signaling through CD28 family molecules plays a crucial role in T-cell activation and immune responses.
  • Human immunodeficiency virus type 1 (HIV-1) infects CD4(+) T-cells, leading to acquired immunodeficiency syndrome (AIDS).
  • Understanding the interplay between immune cell signaling and viral replication is vital for developing therapeutic strategies.

Purpose of the Study:

  • To investigate the impact of CD28 family molecule signaling on HIV-1 replication in vitro.
  • To determine the specific effects of inducible costimulator (ICOS) and CD28 signaling pathways on HIV-1 replication.
  • To explore the potential of ICOS ligands as a therapeutic approach against HIV-1.

Main Methods:

  • Utilized peripheral blood mononuclear cells (PBMC) from healthy donors.
  • Applied monoclonal antibodies (mAbs) specific for ICOS and CD28 to cultured CD4(+) PBMC.
  • Assessed HIV-1 replication using X4 and R5 strains and pseudotype viruses.
  • Measured cell viability, growth, and surface marker expression (CD4, CXCR4, CCR5).
  • Investigated the effects of soluble ligands for ICOS (B7-H2) and CD28 (B7-1).

Main Results:

  • An ICOS-specific mAb significantly suppressed replication of both X4 and R5 HIV-1 strains in CD4(+) PBMC.
  • CD28 mAb also suppressed HIV-1 replication, though with variable effects.
  • Suppression of viral replication was independent of changes in cell growth, viability, or surface marker expression.
  • HIV-1 pseudotype virus entry was inhibited by ICOS and CD28 mAbs.
  • Soluble B7-H2 (ICOS ligand) suppressed HIV-1 replication, while soluble B7-1 (CD28 ligand) enhanced it.

Conclusions:

  • Signaling through ICOS, particularly via its ligand B7-H2, can suppress HIV-1 replication.
  • The antiviral effects of ICOS and CD28 signaling appear to occur primarily at the viral entry stage.
  • ICOS ligands represent a potential therapeutic target for controlling HIV-1 replication.

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