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狒狒疱疹病毒2在小鼠中的神经发病机制与人类感染猕猴疱疹病毒1(B病毒)相似。

Neuropathogenesis of herpesvirus papio 2 in mice parallels infection with Cercopithecine herpesvirus 1 (B virus) in humans.

作者信息

Rogers Kristin M, Ritchey Jerry W, Payton Mark, Black Darla H, Eberle R

机构信息

Department of Veterinary Pathobiology, Center for Veterinary Health Sciences, Oklahoma State University, 250 McElroy Hall, Stillwater, OK 74078-2007, USA.

出版信息

J Gen Virol. 2006 Feb;87(Pt 2):267-276. doi: 10.1099/vir.0.81476-0.

DOI:10.1099/vir.0.81476-0
PMID:16432011
Abstract

Cercopithecine herpesvirus 1 (monkey B virus; BV) produces extremely severe and usually fatal infections when transmitted from macaque monkeys to humans. Cercopithecine herpesvirus 16 (herpesvirus papio 2; HVP2) is very closely related to BV, yet cases of human HVP2 infection are unknown. However, following intramuscular inoculation of mice, HVP2 rapidly invades the peripheral nervous system and ascends the central nervous system (CNS) resulting in death, very much like human BV infections. In this study, the neurovirulence of HVP2 in mice was further evaluated as a potential model system for human BV infections. HVP2 was consistently neurovirulent when administered by epidermal scarification, intracranial inoculation and an eye splash. Quantitative real-time PCR, histopathology and immunohistochemistry were used to follow the temporal spread of virus following skin scarification and to compare the pathogenesis of neurovirulent and apathogenic isolates of HVP2. Apathogenic isolates were found to be capable of reaching the CNS but were extremely inefficient at replicating within the CNS. It is concluded that neurovirulent strains of HVP2 exhibit a pathogenesis in mice that parallels that observed in human BV infections and that this model system may prove useful in dissecting the viral determinants underlying the extreme severity of zoonotic BV infections.

摘要

猕猴疱疹病毒1型(猴B病毒;BV)从猕猴传播给人类时会引发极其严重且通常致命的感染。猕猴疱疹病毒16型(狒狒疱疹病毒2型;HVP2)与BV密切相关,但人类HVP2感染病例尚不清楚。然而,给小鼠肌肉注射后,HVP2会迅速侵入外周神经系统并上行至中枢神经系统(CNS)导致死亡,这与人类BV感染非常相似。在本研究中,进一步评估了HVP2在小鼠中的神经毒力,作为人类BV感染的潜在模型系统。通过表皮划痕、颅内接种和眼部溅入给药时,HVP2始终具有神经毒力。使用定量实时PCR、组织病理学和免疫组织化学来追踪皮肤划痕后病毒的时间传播,并比较HVP2神经毒力和无致病性分离株的发病机制。发现无致病性分离株能够到达CNS,但在CNS内复制的效率极低。得出的结论是,HVP2的神经毒力菌株在小鼠中表现出与人类BV感染中观察到的发病机制相似的情况,并且该模型系统可能有助于剖析人畜共患BV感染极端严重性背后的病毒决定因素。

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