Viruses 2011, 3(7), 1179-1203; doi:10.3390/v3071179

Innate Antiviral Response: Role in HIV-1 Infection

1 Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, 401 North Broadway, Baltimore, MD 21231, USA 2 Department of Molecular Biology and Genetics, Johns Hopkins School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA 3 Department of Biology, Johns Hopkins University, 3400 N Charles St. Baltimore, MD 21218, USA
Received: 24 May 2011; in revised form: 28 June 2011 / Accepted: 29 June 2011 / Published: 14 July 2011
(This article belongs to the Special Issue Antiviral Innate Immunity)
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Abstract: As an early response to infection, cells induce a profile of the early inflammatory proteins including antiviral cytokines and chemokines. Two families of transcriptional factors play a major role in the transcriptional activation of the early inflammatory genes: The well-characterized family of NFkB factors and the family of interferon regulatory factors (IRF). The IRFs play a critical role in the induction of type I interferon (IFN) and chemokine genes, as well as genes mediating antiviral, antibacterial, and inflammatory responses. Type I IFNs represent critical components of innate antiviral immunity. These proteins not only exert direct antiviral effects, but also induce maturation of dendritic cells (DC), and enhance functions of NK, T and B cells, and macrophages. This review will summarize the current knowledge of the mechanisms leading to the innate antiviral response with a focus on its role in the regulation of HIV-1 infection and pathogenicity. We would like this review to be both historical and a future perspective.
Keywords: virus; HIV-1; interferon; IRF; innate immune response

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MDPI and ACS Style

Pitha, P.M. Innate Antiviral Response: Role in HIV-1 Infection. Viruses 2011, 3, 1179-1203.

AMA Style

Pitha PM. Innate Antiviral Response: Role in HIV-1 Infection. Viruses. 2011; 3(7):1179-1203.

Chicago/Turabian Style

Pitha, Paula M. 2011. "Innate Antiviral Response: Role in HIV-1 Infection." Viruses 3, no. 7: 1179-1203.

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