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1994-09-24
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Document 0526
DOCN M9490526
TI Unique lentivirus--host interactions: SIVsmmPBj14 infection of macaques.
DT 9411
AU Fultz PN; Zack PM; Department of Microbiology, University of Alabama at
Birmingham; 35294.
SO Virus Res. 1994 May;32(2):205-25. Unique Identifier : AIDSLINE
MED/94346054
AB The most virulent primate lentivirus identified to date, the simian
virus SIVsmmPBj14 (SIV-PBj14), is unique not only because it causes
acute disease and death within days instead of months or years, but also
because of its replicative and cellular activation properties. The acute
disease syndrome has many features in common with primary HIV-1 disease,
but differences in the respective outcomes of these two acute lentiviral
infections appear to be linked to the rapidity with which SIV-PBj14
replicates and the high titers of virus that subsequently accumulate in
lymphoid tissues. The most prominent pathologic feature of SIV-PBj14 is
extensive lymphoid hyperplasia of T-cell zones, especially in the
gut-associated lymphoid tissue. These expanded T-cell zones contain a
high proportion of lymphoblasts, activated macrophages and syncytial
cells, which are positively correlated with high numbers of SIV
antigen-positive cells. Replication of the virus to high titers,
accompanied by extensive cellular activation and proliferation, leading
to high levels of cytokines, such as interleukin-6 and tumor necrosis
factor-alpha, are consistent with acute inflammatory disease. The
pathogenesis of SIV-PBj14 also appears to correlate most directly with
some of its unique biologic properties, such as the ability to replicate
in resting peripheral blood mononuclear cells, to activate lymphocytes,
and to induce lymphocyte proliferation. Biologically and molecularly
cloned viruses derived from SIV-PBj14 and isolates obtained from macaque
PBj at earlier times, are being used to identify viral determinants that
influence biologic and pathogenic properties of SIV-PBj14. Further
characterization of this virus should provide new insights into
lentivirus-cell interactions and their contributions to disease.
DE Animal Evolution Gastrointestinal System/PATHOLOGY Lymphoid
Tissue/PATHOLOGY Macaca Simian Acquired Immunodeficiency
Syndrome/*ETIOLOGY/PATHOLOGY Support, U.S. Gov't, Non-P.H.S. Support,
U.S. Gov't, P.H.S. SIV/GENETICS/*PATHOGENICITY Virulence JOURNAL
ARTICLE REVIEW REVIEW, TUTORIAL
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).