Small intestine CD4+ T cells are profoundly depleted during acute simian-human immunodeficiency virus infection, regardless of viral pathogenicity

Small intestine CD4+ T cells are profoundly depleted during acute simian-human immunodeficiency virus infection, regardless of viral pathogenicity
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DOI:
10.1128/jvi.02753-07
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发表时间:
2008-06-01
影响因子:
5.4
通讯作者:
Miura, Tomoyuki
Miura, Tomoyuki
中科院分区:
医学2区
文献类型:
--
作者:
Fukazawa, Yoshinori;Miyake, Ariko;Miura, Tomoyuki

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为了分析急性病毒诱导的损伤和随后的疾病表型之间的关系,我们比较了感染同基因高致病性(KS 661)和中等致病性(#64)猴-人免疫缺陷病毒(SHIV)的猴的病毒复制和CD 4(+)T细胞谱。直肠内输注SHIV-KS 661导致快速、全身和大量的病毒复制,而SHIV-#64复制更慢,滴度更低。而KS 661全身性地耗尽CD 4(+)T细胞,#64仅在小肠中引起显著的CD 4(+)T细胞耗尽。我们的结论是,SHIV,无论致病性如何,在急性感染过程中,可引起小肠损伤并导致受感染动物的CD 4(+)T细胞耗竭。
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.