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利用MHV-2和MHV-A59之间的靶向重组研究MHV的嗜神经决定因素。

Targeted recombination between MHV-2 and MHV-A59 to study neurotropic determinants of MHV.

作者信息

Lavi E, Kuo L, Haluskey J A, Masters P S

机构信息

Department of Pathology and Laboratory Medicine, University of Pennsylvania, School of Medicine, Philadelphia 19104, USA.

出版信息

Adv Exp Med Biol. 1998;440:543-7. doi: 10.1007/978-1-4615-5331-1_70.

DOI:10.1007/978-1-4615-5331-1_70
PMID:9782327
Abstract

MHV-A59 produces acute encephalitis, acute hepatitis and chronic demyelination in infected mice. MHV-2 produces only hepatitis and mild meningitis but without encephalitis or demyelination. We have previously studied a set of recombinant viruses between these two strains. The common denominator of viruses that produced encephalitis was a membrane (M) gene derived from MHV-A59. Thus to study the potential contribution of the M gene to acute encephalitis, chimeric viruses were produced in which the M gene of MHV-A59 was substituted with the M gene of MHV-2 by targeted recombination. A control virus was produced in which the M gene of A59 was recombined back into an A59 background. Viruses were then analyzed for their biologic properties and compared with the phenotypes of MHV-A59 and MHV-2 by histopathology and plaque assays for viral titers in organs following intracerebral (IC) inoculation. All three chimeric viruses had a phenotype similar to MHV-A59. Thus, the replacement of the M gene of MHV-A59 with that of MHV-2 is insufficient to produce a phenotype that lacks encephalitis similar to MHV-2.

摘要

MHV - A59在感染的小鼠中会引发急性脑炎、急性肝炎和慢性脱髓鞘。MHV - 2仅引发肝炎和轻度脑膜炎,但不会引发脑炎或脱髓鞘。我们之前研究了这两个毒株之间的一组重组病毒。引发脑炎的病毒的共同特征是其膜(M)基因源自MHV - A59。因此,为了研究M基因对急性脑炎的潜在作用,通过靶向重组构建了嵌合病毒,其中MHV - A59的M基因被MHV - 2的M基因所取代。构建了一种对照病毒,其中A59的M基因被重组回A59背景中。然后对病毒的生物学特性进行分析,并通过组织病理学以及脑内(IC)接种后对器官中病毒滴度的噬斑测定,将其与MHV - A59和MHV - 2的表型进行比较。所有三种嵌合病毒的表型均与MHV - A59相似。因此,用MHV - 2的M基因替换MHV - A59的M基因不足以产生类似于MHV - 2的缺乏脑炎的表型。

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