title: Decay-accelerating factor (CD55) protects human immunodeficiency virus type 1 from inactivation by human complement.
abstract: HIV-1, in contrast to animal retroviruses, is not lysed by human complement, but is readily inactivated by the sera from different animal species. To identify a possible species-specific protection mechanism. HIV-1 was expressed in cells of non-human origin. Recombinant HIV-1 virions that could encode the chloramphenicol acetyltransferase (CAT) protein were produced in African green monkey COS-1 cells, mink cells and, as a control, in human HEp-2 cells and were then used to infect CD4-positive target cells. Analysis of the CAT activity of the target cells revealed that fresh HIV-1-negative human serum reduced the infectivity of HIV-1 derived from monkey and mink cells five- to tenfold, but had no effect on HIV-1 produced in human cells. In addition, human serum efficiently lysed HIV-1 produced in non-human cells in contrast to HIV-1 originating from human cells, suggesting lysis as an important mechanism of virus inactivation. Mammalian cells are protected against lysis by homologous complement by membrane-bound regulatory molecules. Two of these complement inhibitors, namely decay-accelerating factor (DAF) and, to a lesser extent, CD59 were found on the surface of HIV-1 virions by means of a virus capture assay. Antibodies against DAF, but not against other host cell molecules found on the viral surface, efficiently blocked the resistance of HIV-1 produced in human cells to human complement. These results suggest that the acquisition of DAF during the budding process from human cells protects HIV-1 in a species-specific way against the attack of human complement.
authors.affiliation: Institut für Hygiene, Leopold-Franzens-Universität, Innsbruck, Austria.
authors.forename: P
authors.initials: P
authors.lastname: Marschang
authors.forename: J
authors.initials: J
authors.lastname: Sodroski
authors.forename: R
authors.initials: R
authors.lastname: Würzner
authors.forename: M P
authors.initials: MP
authors.lastname: Dierich
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000502:physiology*; D018958:CD55 Antigens; D002460:Cell Line; D002461:Cell Line, Transformed; D002522:Chlorocebus aethiops; D003169:Complement Inactivator Proteins / Q000502:physiology*; D003165:Complement System Proteins / Q000276:immunology*; D016655:HIV Core Protein p24 / Q000276:immunology; D054303:HIV Reverse Transcriptase; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D008562:Membrane Glycoproteins / Q000502:physiology*; D008907:Mink; D012194:RNA-Directed DNA Polymerase / Q000378:metabolism; D014407:Tumor Cells, Cultured
chemical_list: D015703:Antigens, CD; D018958:CD55 Antigens; D003169:Complement Inactivator Proteins; D016655:HIV Core Protein p24; D008562:Membrane Glycoproteins; D003165:Complement System Proteins; D054303:HIV Reverse Transcriptase; D012194:RNA-Directed DNA Polymerase