Growth failure and AIDS-like cachexia syndrome in HIV-1 transgenic mice.
Journal Article (Journal Article)
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.
Full Text
Duke Authors
Cited Authors
- Santoro, TJ; Bryant, JL; Pellicoro, J; Klotman, ME; Kopp, JB; Bruggeman, LA; Franks, RR; Notkins, AL; Klotman, PE
Published Date
- May 15, 1994
Published In
Volume / Issue
- 201 / 1
Start / End Page
- 147 - 151
PubMed ID
- 7909972
International Standard Serial Number (ISSN)
- 0042-6822
Digital Object Identifier (DOI)
- 10.1006/viro.1994.1276
Language
- eng
Conference Location
- United States