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Inhibition of human immunodeficiency virus type 1 replication prior to reverse transcription by influenza virus stimulation

  1. Author:
    Pinto, L. A.
    Blazevic, V.
    Patterson, B. K.
    Mac Trubey, C.
    Dolan, M. J.
    Shearer, G. M.

  2. Author Address

    Shearer GM NCI, Expt Immunol Branch, NIH Bldg 10,Rm 4B36 Bethesda, MD 20892 USA NCI, Expt Immunol Branch, NIH Bethesda, MD 20892 USA NCI, FCRDC, SAIC Frederick, Intramural Res Support Program Frederick, MD USA Northwestern Univ, Sch Med, Lab Viral Pathogenesis Chicago, IL 60611 USA Wilford Hall USAF Med Ctr Lackland AFB, TX 78236 USA
    1. Year: 2000
  2. Journal: Journal of Virology
    1. 74
    2. 10
    3. Pages: 4505-4511
  4. Type of Article: Article
  1. Abstract:

    It is now recognized that, in addition to drug-mediated therapies against human immunodeficiency virus type 1 (HIV-1), the immune system can exert antiviral effects via CD8(+) T-cell-generated anti-HIV factors. This study demonstrates that (i) supernatants from peripheral blood mononuclear cells (PBMC) stimulated with influenza A virus inhibit replication of CCR5- and CXCR4-tropic HIV-1 isolates prior to reverse transcription; (ii) the HIV-suppressive supernatants can be generated by CD4- or CD8-depleted PBMC; (iii) this anti-HIV activity is partially due to alpha interferon (IFN-alpha), but not to IFN-gamma, IFN-beta, the beta-chemokines MIP-1 alpha, MIP-1 beta, and RANTES, or interleukin-16; (iv) the anti-HIV activity is generated equally well by PBMC cultured with either infectious or UV-inactivated influenza A virus; and (v) the antiviral activity can be generated by influenza A-stimulated PBMC from HN-infected individuals. These findings represent a novel mechanism for inhibition of HIV-1 replication that differs from the previously described CD8 anti-HIV factors (MIP-la, MIP-1 beta, RANTES, and CD8 antiviral factor). [References: 41]

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