       Document 0624
 DOCN  M9630624
 TI    HIV-1 mediates rapid apoptosis of lymphocytes from human CD4 transgenic
       but not normal rabbits.
 DT    9603
 AU    Leno M; Hague BF; Teller R; Kindt TJ; Laboratory of Immunogenetics,
       National Institute of Allergy and; Infectious Diseases, National
       Institutes of Health, Rockville,; Maryland 20852, USA.
 SO    Virology. 1995 Nov 10;213(2):450-4. Unique Identifier : AIDSLINE
       MED/96074520
 AB    Normal rabbit lymphocytes can be infected with HIV-1 although infection
       is much less efficient than in human lymphocytes. When peripheral blood
       mononuclear cells (PBMC) from rabbits transgenic for human CD4 (HuCD4)
       were exposed to HIV-1, enhanced infection and a rapid depletion of
       lymphocytes were observed. Cell death in the infected cultures occurred
       via apoptosis, but no similar effect was seen in nontransgenic rabbit
       PBMC cultures. Induction of apoptosis in HuCD4-expressing cells required
       virus replication; heat-inactivated virus or recombinant viral proteins
       had no effect on cell viability. Expression of the Fas antigen was
       increased in HIV-1-infected CD4+ rabbit lymphocytes. Characterization of
       the infected PBMC cultures revealed that apoptosis occurs both in HuCD4+
       and HuCD4- cells, indicating that bystander cells are killed. These data
       define a requirement for HuCD4 in initiation, but not the spread, of
       HIV-1-induced apoptosis in rabbit PBMC and provide a model to probe
       mechanisms leading to lymphocyte depletion in HIV-1 infection.
 DE    Animal  Animals, Transgenic  Antigens, CD4/*ANALYSIS  Antigens,
       CD95/BIOSYNTHESIS  Apoptosis/*PHYSIOLOGY  Cells, Cultured  Comparative
       Study  Human  HIV-1/*PHYSIOLOGY
       Lymphocytes/*CYTOLOGY/IMMUNOLOGY/*VIROLOGY  Rabbits  Receptors,
       Interleukin-2/BIOSYNTHESIS  Up-Regulation (Physiology)  JOURNAL ARTICLE

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

