Document 0194 DOCN M9460194 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).