title: Innate immunity in resistance to HIV infection.
abstract: Resistance to human immunodeficiency virus (HIV) infection in subjects who do not seroconvert despite multiple exposures to the virus and to the progression to AIDS in HIV&#x2010;infected individuals depends on multiple factors involving both the innate and the adaptive immune system. The contribution of natural immunity in preventing HIV infection has so far received little attention, but many recently published articles suggest a key role for Toll&#x2010;like receptors, natural killer cells, interleukin&#x2010;22, acute&#x2010;phase amyloid A protein, and APOBEC3G in conferring resistance to HIV infection. The study of these factors will shed light on HIV pathogenesis and contribute to the development of new therapeutic approaches to this elusive disease.
authors.affiliation: Department of Clinical Sciences, University of Milano, Milan, Italy. mara.biasin@unimi.it
authors.forename: Mara
authors.initials: M
authors.lastname: Biasin
authors.forename: Mario
authors.initials: M
authors.lastname: Clerici
authors.forename: Luca
authors.initials: L
authors.lastname: Piacentini
mesh_terms: D000071480:APOBEC-3G Deaminase; D003564:Cytidine Deaminase / Q000276:immunology; D006678:HIV / Q000276:immunology*; D015658:HIV Infections / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate; D007378:Interleukins / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology; D000685:Serum Amyloid A Protein / Q000276:immunology; D051193:Toll-Like Receptors / Q000276:immunology; D000097043:Interleukin-22
chemical_list: D000071480:APOBEC-3G Deaminase; D003564:Cytidine Deaminase; D007378:Interleukins; D000685:Serum Amyloid A Protein; D051193:Toll-Like Receptors; D000097043:Interleukin-22; C464924:APOBEC3G protein, human