Document 0601
 DOCN  M9550601
 TI    Reactivation of human immunodeficiency virus type 2 in macaques after
       simian immunodeficiency virus SIVmac superinfection.
 DT    9505
 AU    Petry H; Dittmer U; Stahl-Hennig C; Coulibaly C; Makoschey B; Fuchs D;
       Wachter H; Tolle T; Morys-Wortmann C; Kaup FJ; et al; Department of
       Virology and Immunology, German Primate Centre,; Gottingen.
 SO    J Virol. 1995 Mar;69(3):1564-74. Unique Identifier : AIDSLINE
       MED/95156582
 AB    By superinfection of human immunodeficiency virus type 2 (HIV-2) strain
       HIV-2ben-infected macaques with simian immunodeficiency virus (SIV)
       strain SIVmac, we investigated the mutual influences of an apathogenic
       and a pathogenic virus in vivo. Four rhesus and two cynomolgus monkeys
       were infected with HIV-2ben in 1988 and 1989, respectively. Virus could
       be reisolated from five of six animals 6 weeks after infection. The
       monkeys remained healthy over the next 2 to 3 years. PCR for viral RNA
       became negative, and virus could no longer be reisolated by coculture.
       All six macaques were superinfected with the pathogenic SIVmac251/32H.
       Subsequently, five monkeys became persistently viremic, while one animal
       was protected against the SIVmac infection. In the peripheral blood
       mononuclear cells and cocultures of the five viremic animals, DNA from
       both HIV-2 and SIVmac was present. The plasma contained RNA from both
       viruses. Thus, superinfection with SIVmac activated HIV-2. A
       proliferative T-cell response against both HIV-2 and SIVmac was measured
       in all animals after superinfection. Such a response was regularly seen
       after infection with the apathogenic HIV-2 but never when the pathogenic
       SIVmac alone was administered. While naive control monkeys inoculated
       with SIVmac251/32H regularly develop AIDS-like symptoms soon after
       infection and have to be killed, none of the preinfected animals has
       developed AIDS-like symptoms, but two of six animals developed tumors.
       After the SIVmac challenge, however, apoptotic lymphocytes were detected
       in the peripheral blood mononuclear cells of all animals. Thus, the
       presence of an apathogenic viral variant seems to retard the disease
       occurring after infection with a pathogenic virus rather than to confirm
       total protection. This partial protection appears to depend on a
       specific proliferative T-cell response early after infection.
 DE    Animal  Apoptosis  Base Sequence  DNA Primers/CHEMISTRY  DNA,
       Viral/GENETICS  Gene Expression Regulation, Viral  HIV
       Antibodies/IMMUNOLOGY  HIV Antigens/IMMUNOLOGY  HIV Infections/*GENETICS
       HIV-2/GENETICS/*PATHOGENICITY  Lymphocyte Transformation  Macaca mulatta
       Molecular Sequence Data  Proviruses/GENETICS  RNA, Messenger/GENETICS
       RNA, Viral/GENETICS  Simian Acquired Immunodeficiency
       Syndrome/*GENETICS/MICROBIOLOGY  SIV/GENETICS/*PATHOGENICITY
       T-Lymphocytes, Helper-Inducer/IMMUNOLOGY  Time Factors  Virus
       Replication  JOURNAL ARTICLE

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