Document 0399
 DOCN  M9550399
 TI    Decay-accelerating factor (CD55) protects human immunodeficiency virus
       type 1 from inactivation by human complement.
 DT    9505
 AU    Marschang P; Sodroski J; Wurzner R; Dierich MP; Institut fur Hygiene,
       Leopold-Franzens-Universitat, Innsbruck,; Austria.
 SO    Eur J Immunol. 1995 Jan;25(1):285-90. Unique Identifier : AIDSLINE
       MED/95145542
 AB    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.
 DE    Animal  Antigens, CD/*PHYSIOLOGY  Cell Line  Cell Line, Transformed
       Cercopithecus aethiops  Complement/*IMMUNOLOGY  Complement
       Inactivators/*PHYSIOLOGY  Human  HIV Core Protein p24/IMMUNOLOGY
       HIV-1/*IMMUNOLOGY  Membrane Glycoproteins/*PHYSIOLOGY  Mink  Reverse
       Transcriptase/METABOLISM  Support, Non-U.S. Gov't  Support, U.S. Gov't,
       P.H.S.  Tumor Cells, Cultured  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).