title: Type I interferon: understanding its role in HIV pathogenesis and therapy.
abstract: Despite over 30 years of research, the contribution of type I interferons (IFN-Is) to both the control of HIV replication and initiation of immunologic damage remains debated. In acute infection, IFN-Is, likely from plasmacytoid dendritic cells (pDCs), activate NK cells and upregulate restriction factors targeting virtually the entire HIV life cycle. In chronic infection, IFN-Is may also contribute to CD4 T cell loss and immune exhaustion. pDCs subsequently infiltrate lymphoid and mucosal tissues, and their circulating populations wane in chronic infection; IFN-I may be produced by other cells. Data from nonhuman primates indicate prompt IFN-I signaling is critical in acute infection. Whereas some studies showed IFN-I administration without combination antiretroviral therapy (cART) is beneficial, others suggest that stimulating or blocking IFN-I signaling in chronic ART-suppressed HIV infection has had positive results. Here, we describe the history of HIV and IFN-I, IFN-I's sources, IFN-I's effects on HIV control and host defense, and recent interventional studies in SIV and HIV infection.
authors: Division of Microbiology and Immunology, Emory Vaccine Center, Yerkes National Primate Research Center, Emory Vaccine Center Bldg. 3028, Atlanta, GA, 30322, USA, steven.bosinger@emory.edu.
authors: Steven E
authors: SE
authors: Bosinger
authors: Netanya S
authors: NS
authors: Utay
mesh_terms: D000818:Animals; D000998:Antiviral Agents; D015658:HIV Infections / Q000188:drug therapy* / Q000209:etiology*; D006801:Humans; D007111:Immunity, Cellular; D007370:Interferon Type I / Q000502:physiology*; D007694:Killer Cells, Natural / Q000502:physiology; D023421:Models, Animal
chemical_list: D000998:Antiviral Agents; D007370:Interferon Type I