Fukazawa Yoshinori, Miyake Ariko, Ibuki Kentaro, Inaba Katsuhisa, Saito Naoki, Motohara Makiko, Horiuchi Reii, Himeno Ai, Matsuda Kenta, Matsuyama Megumi, Takahashi Hidemi, Hayami Masanori, Igarashi Tatsuhiko, Miura Tomoyuki
Laboratory of Primate Model, Experimental Research Center for Infectious Diseases, Institute for Virus Research, Kyoto University, 53 Shogoinkawaramachi, Sakyo-ku, Kyoto 606-8507, Japan.
J Virol. 2008 Jun;82(12):6039-44. doi: 10.1128/JVI.02753-07. Epub 2008 Apr 9.
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.
为了分析急性病毒诱导的损伤与随后疾病表型之间的关系，我们比较了感染同基因高致病性（KS661）和中度致病性（#64）猴免疫缺陷病毒（SHIV）的猴子的病毒复制情况和CD4(+) T细胞谱。经直肠注入SHIV-KS661导致快速、全身性和大量的病毒复制，而SHIV-#64复制较慢且滴度较低。KS661使CD4(+) T细胞在全身耗竭，而#64仅在小肠中导致显著的CD4(+) T细胞耗竭。我们得出结论，无论致病性如何，SHIV在急性感染期间均可导致感染动物的小肠损伤并导致CD4(+) T细胞耗竭。
