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1994-09-19
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Document 0421
DOCN M9490421
TI Immune activation and viral burden in acute disease induced by simian
immunodeficiency virus SIVsmmPBj14: correlation between in vitro and in
vivo events.
DT 9411
AU Schwiebert R; Fultz PN; Department of Microbiology, University of
Alabama at Birmingham; 35294.
SO J Virol. 1994 Sep;68(9):5538-47. Unique Identifier : AIDSLINE
MED/94335066
AB The simian immunodeficiency virus SIVsmmPBj14 (SIV-PBj14) is an atypical
lentivirus that causes acute disease and death in pig-tailed macaques
and in vitro replicates efficiently in resting macaque lymphocytes and
activates and induces proliferation of lymphocytes. The present study
was conducted to test the hypothesis that production of large quantities
of SIV-PBj14 induces widespread immune activation and elaboration of
cytokines which lead directly to the death of infected pig-tailed
macaques. Following intravenous inoculation of pig-tailed macaques with
SIV-PBj14, acute disease developed and was characterized by high levels
of plasma viremia, p27gag antigenemia, tumor necrosis factor alpha, and
interleukin-6 (IL-6). All animals died within 10 days of infection, at
which time some animals had as many as 100% CD4+ cells in the periphery
and lymphoid tissues infected. During the last few days before death,
titers of infectious virus in blood increased as much as 10(5)-fold. By
using dual-label immunofluorescence assays for detection of cell surface
activation markers, both CD4+ and CD8+ lymphocytes were shown to express
the IL-2 and transferrin receptors following either in vivo or in vitro
infection with SIV-PBj14. Furthermore, in vitro infection of quiescent
macaque lymphocytes by SIV-PBj14 was accompanied by proliferation of
both CD4+ and CD8+ lymphocyte subsets, as measured by incorporation of
[3H]thymidine. Increases in numbers of activated lymphocytes and levels
of proinflammatory cytokines in plasma coincided with increased amounts
of detectable virus in vivo. Clinical signs of disease and pathologic
findings were most consistent with death from a shock-like syndrome, in
which acute-phase inflammatory cytokines are known to play a major role.
Tumor necrosis factor alpha, IL-2, and IL-6 were detected in some
cultures infected with SIV-PBj14, but this finding was not consistent.
When cytokines were detected, their concentrations were essentially no
different from those found in control cultures infected with SIVsmm9, a
prototypic strain from which SIV-PBj14 was derived. The in vivo results
suggest a synergistic cycle of activation of lymphocytes and monocytes,
elaboration of cytokines, and virus production that accelerates
uncontrolled and culminates in death. The observed correlations between
in vivo and in vitro activation events following SIV-PBj14 infection
validate the use of in vitro studies to clarify lentivirus-lymphocyte
interactions that may contribute to the virulence of SIV-PBj14.
DE Animal Antigens, CD/ANALYSIS Antigens, Differentiation,
B-Lymphocyte/ANALYSIS CD4-CD8 Ratio Interleukin-6/METABOLISM
Lymphocyte Transformation Macaca nemestrina Receptors,
Interleukin-2/ANALYSIS Simian Acquired Immunodeficiency
Syndrome/*IMMUNOLOGY/ MICROBIOLOGY Support, U.S. Gov't, P.H.S.
SIV/*IMMUNOLOGY Tumor Necrosis Factor/METABOLISM Virus Replication
JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).