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由于先前用复制缺陷型DY株进行外周接种,可传播水貂脑病HY株的朊病毒病发病延迟。

Delay in onset of prion disease for the HY strain of transmissible mink encephalopathy as a result of prior peripheral inoculation with the replication-deficient DY strain.

作者信息

Bartz Jason C, Aiken Judd M, Bessen Richard A

机构信息

Department of Medical Microbiology and Immunology, Creighton University, Omaha, NE 68178, USA.

Department of Animal Health and Biomedical Sciences, University of Wisconsin, Madison, WI 53706, USA.

出版信息

J Gen Virol. 2004 Jan;85(Pt 1):265-273. doi: 10.1099/vir.0.19394-0.

DOI:10.1099/vir.0.19394-0
PMID:14718642
Abstract

We report that the replication-deficient DY strain of transmissible mink encephalopathy (TME) can delay disease caused by the pathogenic HY TME strain. In this study, competition between the HY and DY TME agents was investigated following superinfection of the sciatic nerve and peritoneal cavity. Initially, DY TME infection was examined in the absence of superinfection and it was found that inoculation into the brain and sciatic nerve resulted in prion disease and PrP(Sc) deposition in brain but not lymphoreticular tissues. Conversely, intraperitoneal inoculation of the DY TME agent did not result in clinical symptoms, DY TME agent replication or PrP(Sc) deposition 400-600 days after infection. These findings indicate that the DY TME agent does not replicate in secondary lymphoid organs and is non-pathogenic when neuroinvasion is dependent on prior infection of the lymphoreticular system. However, intraperitoneal inoculation of the DY TME agent at 60 days, but not at 30 days, prior to intraperitoneal inoculation of the HY TME agent resulted in an extension of the HY TME incubation period. Inoculation of the DY TME agent into the sciatic nerve at 60 days prior to intrasciatic nerve inoculation of the HY TME agent did not delay the incubation period of HY TME. The ability of the DY TME agent to delay HY TME infection following extraneural inoculation, but not neural infection, suggests that HY and DY TME agent competition can occur in a common replication site whose cellular location precedes infection of both the lymphoreticular and peripheral nervous systems.

摘要

我们报告称,可传播的水貂脑病(TME)的复制缺陷型DY毒株能够延缓致病性HY TME毒株引发的疾病。在本研究中,在坐骨神经和腹腔进行重复感染后,对HY和DY TME病原体之间的竞争进行了研究。最初,在不存在重复感染的情况下检测了DY TME感染,发现接种到脑和坐骨神经中会导致朊病毒病以及脑中PrP(Sc)沉积,但在淋巴网状组织中不会出现。相反,腹腔接种DY TME病原体在感染后400 - 600天未导致临床症状、DY TME病原体复制或PrP(Sc)沉积。这些发现表明,DY TME病原体在次级淋巴器官中不复制,并且当神经侵袭依赖于淋巴网状系统的先前感染时是非致病性的。然而,在腹腔接种HY TME病原体前60天而非30天腹腔接种DY TME病原体,会导致HY TME潜伏期延长。在坐骨神经接种HY TME病原体前60天将DY TME病原体接种到坐骨神经中,并未延缓HY TME的潜伏期。DY TME病原体在非神经接种而非神经接种后延缓HY TME感染的能力表明,HY和DY TME病原体竞争可能发生在一个共同的复制位点,其细胞定位先于淋巴网状系统和周围神经系统的感染。

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