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Published on: August 13, 2013

Immunodeficiency virus cDNA synthesis in resting T lymphocytes is regulated by T cell activation signals and

P S Polacino1, L M Pinchuk, S P Sidorenko

  • 1Washington Regional Primate Research Center, University of Washington, Seattle 98195, USA.

Journal of Medical Primatology
|June 1, 1996
PubMed

Insights

Viral replication in T cells depends on cell cycle progression and dendritic cell (DC) interactions. Mimosine blocked simian immunodeficiency virus (SIV) circularization, indicating G1 phase involvement, while DC receptor activation influenced human immunodeficiency virus (HIV) spread.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • T cell activation and dendritic cell (DC) interactions are crucial for immunodeficiency virus replication.
  • Understanding the cell cycle's role in viral DNA synthesis is key to developing antiviral strategies.

Purpose of the Study:

  • To investigate the impact of cell cycle regulation on SIV DNA synthesis in T cells.
  • To characterize the role of DCs and specific surface receptors (IPO-3, Bgp95) in HIV-1 replication.

Main Methods:

  • Macaque resting T cells were infected with SIV in the presence of cell cycle inhibitors (mimosine, aphidicolin).
  • SIV reverse transcription, circularization, and integration were analyzed.
  • Human T cells were co-cultured with DCs, and HIV-1 expression was measured after receptor ligation (IPO-3, Bgp95).

Main Results:

  • Mimosine, a G1 inhibitor, blocked SIV LTR circle formation, suggesting G1 phase signaling is critical.
  • Aphidicolin, a G1/S inhibitor, did not affect SIV circularization or integration.
  • Activation of DCs via IPO-3 and Bgp95 receptors upregulated HIV spread; IPO-3 activation alone on T cells also increased HIV-1 levels.

Conclusions:

  • SIV LTR circle production is linked to signaling events regulating the G1 to S phase transition.
  • DC activation through specific receptors, particularly IPO-3, enhances HIV-1 replication.
  • T cell activation, either via surface receptors or DCs, is essential for initiating HIV/SIV cDNA synthesis.

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