Previous Article | Next Article ![]()
Journal of Virology, June 2008, p. 6039-6044, Vol. 82, No. 12
0022-538X/08/$08.00+0 doi:10.1128/JVI.02753-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Ariko Miyake,1,2,
Kentaro Ibuki,1
Katsuhisa Inaba,1
Naoki Saito,1
Makiko Motohara,1
Reii Horiuchi,1
Ai Himeno,1
Kenta Matsuda,1
Megumi Matsuyama,1
Hidemi Takahashi,3
Masanori Hayami,1
Tatsuhiko Igarashi,1 and
Tomoyuki Miura1*
Laboratory of Primate Model, Experimental Research Center for Infectious Diseases, Institute for Virus Research, Kyoto University, 53 Shogoinkawaramachi, Sakyo-ku, Kyoto 606-8507, Japan,1 Laboratory of Tumor Cell Biology, Department of Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo 162-8640, Japan,2 Department of Microbiology and Immunology, Nippon Medical School, Tokyo 113-8602, Japan3
Received 27 December 2007/ Accepted 27 March 2008
To analyze the relationship between acute virus-induced injury and the subsequent disease phenotype, we compared the virus replication and CD4+ T-cell profiles for monkeys infected with isogenic highly pathogenic (KS661) and moderately pathogenic (#64) simian-human immunodeficiency viruses (SHIVs). Intrarectal infusion of SHIV-KS661 resulted in rapid, systemic, and massive virus replication, while SHIV-#64 replicated more slowly and reached lower titers. Whereas KS661 systemically depleted CD4+ T cells, #64 caused significant CD4+ T-cell depletion only in the small intestine. We conclude that SHIV, regardless of pathogenicity, can cause injury to the small intestine and leads to CD4+ T-cell depletion in infected animals during acute infection.
Published ahead of print on 9 April 2007.
These authors contributed equally to this work.
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»