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Specific Marking of HIV-1 Positive Cells using a Rev-dependent Lentiviral Vector Expressing the Green Fluorescent Protein
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Trans-activation of HIV-1 LTR-directed gene expression by tat requires protein kinase C

A Jakobovits1, A Rosenthal, D J Capon

  • 1Department of Molecular Biology, Genentech, Inc., South San Francisco, CA 94080.

The EMBO Journal
|April 1, 1990
PubMed

Insights

Protein Kinase C (PKC) is crucial for activating latent Human Immunodeficiency Virus (HIV). Depleting PKC inhibits HIV transactivation, suggesting PKC

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Latent Human Immunodeficiency Virus (HIV) integrated into the host genome is a major challenge for eradication.
  • HIV-1 latency is established by integrated provirus, requiring specific cellular signals for reactivation.
  • The HIV-1 tat protein is a potent transactivator of viral gene expression, critical for viral replication.

Purpose of the Study:

  • To investigate the role of Protein Kinase C (PKC) in the activation of latent HIV-1.
  • To determine if PKC regulates HIV-1 transactivation independently of tat protein synthesis.
  • To elucidate the mechanism by which mitogenic stimulation induces HIV-1 transactivation.

Main Methods:

  • Depletion of Protein Kinase C (PKC) in T cells.
  • Assessing HIV-1 transactivation levels in PKC-depleted cells.
  • Restoration of transactivation by transfecting PKC expression vectors.
  • Analyzing the involvement of PMA-responsive enhancer elements.

Main Results:

  • Depletion of PKC significantly reduced HIV-1 transactivation.
  • Tat protein synthesis was unaffected by PKC depletion.
  • Transactivation was restored in PKC-depleted cells upon PKC reintroduction.
  • PKC's role in transactivation did not involve PMA-responsive enhancer elements.

Conclusions:

  • Protein Kinase C (PKC) plays a critical regulatory role in HIV-1 transactivation.
  • PKC mediates mitogen-induced activation of HIV-1, independent of tat synthesis.
  • This highlights a key pathway in the transition of HIV from latency to productive infection.

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