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


  • eng

Conference Location

  • United States