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In Vitro Assay to Evaluate the Impact of Immunoregulatory Pathways on HIV-specific CD4 T Cell Effector Function
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Published on: October 16, 2013

Interferon alpha-mediated inhibition of human immunodeficiency virus type 1 provirus synthesis in T-cells

Y Shirazi1, P M Pitha

  • 1Oncology Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231.

Virology
|March 1, 1993
PubMed

Insights

Interferon-alpha (IFN-alpha) significantly inhibits human immunodeficiency virus type-1 (HIV-1) replication by blocking provirus formation. This antiviral effect stems from IFN-alpha interfering with the initiation of HIV-1 reverse-transcription.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Interferon-alpha (IFN-alpha) is known to inhibit human immunodeficiency virus type-1 (HIV-1) replication in cell lines.
  • The precise mechanism of IFN-alpha's antiviral activity against HIV-1 requires further elucidation.

Purpose of the Study:

  • To investigate the specific stage at which IFN-alpha inhibits HIV-1 replication.
  • To determine if IFN-alpha affects provirus formation and reverse-transcription.

Main Methods:

  • Polymerase chain reaction (PCR) was used to detect HIV-1 proviral DNA in infected cells.
  • Primers were designed to detect complete or nearly complete proviral DNA and early reverse-transcripts.
  • In vitro assays were performed using cytoplasmic extracts from IFN-alpha-treated cells to assess reverse transcriptase activity.

Main Results:

  • IFN-alpha pretreatment significantly reduced the levels of HIV-1 proviral DNA in infected cells.
  • IFN-alpha was found to interfere with the initiation of HIV-1 reverse-transcription.
  • Cytoplasmic extracts from IFN-alpha-treated cells inhibited HIV-1 reverse transcriptase activity in vitro.

Conclusions:

  • IFN-alpha inhibits HIV-1 replication by blocking provirus formation at the level of reverse-transcription initiation.
  • IFN-alpha demonstrates therapeutic potential for limiting the spread of HIV-1 infection.

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