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M9460575.TXT
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1994-06-25
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Document 0575
DOCN M9460575
TI Growth failure and AIDS-like cachexia syndrome in HIV-1 transgenic mice.
DT 9408
AU Santoro TJ; Bryant JL; Pellicoro J; Klotman ME; Kopp JB; Bruggeman LA;
Franks RR; Notkins AL; Klotman PE; Department of Medicine, University of
Colorado Health Sciences; Center, Denver 80220.
SO Virology. 1994 May 15;201(1):147-51. Unique Identifier : AIDSLINE
MED/94233764
AB The mechanisms which predispose to growth failure in infants and
children infected with immunodeficiency virus type-1 (HIV-1) are not
fully understood. The contributions of viral replication and CD4+ T cell
depletion to growth failure in an HIV-1 transgenic mouse model were
investigated. Mice homozygous for the transgene, a gag-pol deletion
mutant of the HIV-1 provirus pNL4-3, exhibited marked cachexia, growth
retardation, lymphoproliferation with a reduction in the percentage of
CD4+ T cells but an increase in the absolute number of splenic CD4+ and
CD8+ T cells, thymic hypoplasia, and early death. Despite the absence of
T cells, athymic nude mice, homozygous for the HIV transgene, displayed
comparable growth failure. The results indicate that AIDS-like cachexia
may be produced by expression of viral envelope or accessory genes, need
not be accompanied by absolute depletion of CD4+ T cells, and may occur
independent of T cell function.
DE Acquired Immunodeficiency Syndrome/IMMUNOLOGY/*MICROBIOLOGY/
PHYSIOPATHOLOGY Animal Animals, Newborn Body Weight
Cachexia/IMMUNOLOGY/*MICROBIOLOGY/PHYSIOPATHOLOGY Female Fusion
Proteins, gag-pol/GENETICS Gene Expression Gene Products, nef/ANALYSIS
*Genes, Viral Homozygote HIV-1/*GENETICS Immunophenotyping Male
Mice Mice, Transgenic RNA, Viral/ANALYSIS T4 Lymphocytes/*IMMUNOLOGY
JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).