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恒河猴体内猿猴免疫缺陷病毒的直肠内传播:短暂或持续病毒血症的选择性扩增及宿主反应

Intrarectal transmission of simian immunodeficiency virus in rhesus macaques: selective amplification and host responses to transient or persistent viremia.

作者信息

Trivedi P, Horejsh D, Hinds S B, Hinds PW I I, Wu M S, Salvato M S, Pauza C D

机构信息

Department of Pathology, University of Wisconsin, Madison 53706, USA.

出版信息

J Virol. 1996 Oct;70(10):6876-83. doi: 10.1128/JVI.70.10.6876-6883.1996.

Abstract

Intrarectal simian immunodeficiency virus (SIV) infection in rhesus macaques is a model for sexual transmission of primate retroviruses. Phylogenetic studies on envelope gene sequences that were present in blood following intrarectal SIV inoculation provided evidence for selective amplification of a subset of viruses present in the inoculum and defined one amino acid sequence uniquely associated with intrarectal infection. Both persistent and transient viremia states were observed after intrarectal infection. Immune responses in persistently infected animals accounted for slower rates of disease progression despite the presence of highly pathogenic viruses that were documented by transfusion studies. Transient viremia elicited protective immunity against subsequent intrarectal virus challenge but did not protect against intravenous virus challenge. Transient viremia usually but not always led to self-limiting infection. In one animal, we documented a relapse to active viremia long after the initial transient viremia. SIV transmission across mucosal barriers affects pathogenesis in the short term by limiting the types of viruses established in the host and in the longer term by establishing host responses that slow disease progression despite the presence of highly pathogenic viruses in blood.

摘要

恒河猴直肠内感染猿猴免疫缺陷病毒(SIV)是灵长类逆转录病毒性传播的一种模型。对直肠内接种SIV后血液中存在的包膜基因序列进行的系统发育研究,为接种物中存在的一部分病毒的选择性扩增提供了证据,并确定了一个与直肠内感染独特相关的氨基酸序列。直肠内感染后观察到了持续性和短暂性病毒血症状态。尽管输血研究证明存在高致病性病毒,但持续感染动物的免疫反应导致疾病进展速度较慢。短暂性病毒血症引发了针对随后直肠内病毒攻击的保护性免疫,但不能预防静脉内病毒攻击。短暂性病毒血症通常但并非总是导致自限性感染。在一只动物中,我们记录到在最初的短暂性病毒血症很久之后,病毒血症复发至活跃状态。SIV跨黏膜屏障的传播在短期内通过限制宿主体内确立的病毒类型影响发病机制,而在长期内通过建立宿主反应来减缓疾病进展,尽管血液中存在高致病性病毒。

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