Document 0701
 DOCN  M9480701
 TI    CD8+ T lymphocytes of African green monkeys secrete an immunodeficiency
       virus-suppressing lymphokine.
 DT    9410
 AU    Ennen J; Findeklee H; Dittmar MT; Norley S; Ernst M; Kurth R;
       Paul-Ehrlich Institute, Langen, Germany.
 SO    Proc Natl Acad Sci U S A. 1994 Jul 19;91(15):7207-11. Unique Identifier
       : AIDSLINE MED/94316666
 AB    Following natural and experimental infection by simian immunodeficiency
       virus SIVagm of African green monkeys (AGMs), the natural host, there is
       no evidence for the development of an immunodeficiency. Within the
       framework of our studies on human immunodeficiency virus (HIV)/SIV
       pathogenesis, we investigated the influence of CD8 T lymphocytes on
       SIVagm replication in AGM CD4 T lymphocytes in vitro. The following
       observations were made: (i) Peripheral blood mononuclear cells from both
       seronegative and seropositive AGMs contained only a low proportion
       (i.e., 10%) of CD4+ lymphocytes, whereas a high proportion (80%) of CD8+
       cells was detected. Even after persistent SIVagm infection, CD4 T
       lymphocytes do not decrease in number. (ii) The target of in vitro
       infection of peripheral blood cells is the CD4+ mononuclear cell (T
       lymphocytes, monocytes) and SIVagm infects by binding to the CD4
       molecule. (iii) In both naturally and experimentally SIVagm-infected
       AGMs the CD4+ T cells and monocytes, but not the CD8+ T cells, harbor
       DNA provirus. (iv) Virus reisolation and virus replication of SIVagm in
       CD4 T lymphocytes from seropositive AGMs is suppressed in the presence
       of autologous CD8 T lymphocytes or a soluble factor produced by these
       cells. Taken together, one possible reason for the apathogenicity of the
       SIVagm infection in AGMs may be the suppression of virus replication by
       a soluble, yet unidentified factor secreted by CD8 lymphocytes
       quantitatively dominating among peripheral blood cell populations. We
       have tentatively termed this factor immunodeficiency virus-suppressing
       lymphokine. In addition, we show that immunodeficiency virus-suppressing
       lymphokine from AGMs is able to suppress HIV-1 replication in human CD4+
       T cells.
 DE    Animal  Antigens, CD8  Base Sequence  Cercopithecus aethiops  DNA,
       Viral/ANALYSIS  Lymphokines/IMMUNOLOGY/*SECRETION  Molecular Sequence
       Data  Monocytes/CYTOLOGY/MICROBIOLOGY  Proviruses/GENETICS  Simian
       Acquired Immunodeficiency Syndrome/*IMMUNOLOGY  Support, Non-U.S. Gov't
       SIV/*IMMUNOLOGY/PHYSIOLOGY  T-Lymphocyte
       Subsets/IMMUNOLOGY/MICROBIOLOGY/*SECRETION  T4 Lymphocytes/MICROBIOLOGY
       Virus Replication  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
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