在持续感染MHV - A59的小鼠中，中枢神经系统脱髓鞘既不需要B细胞也不需要T细胞。
Neither B cells nor T cells are required for CNS demyelination in mice persistently infected with MHV-A59.
作者信息
Matthews A E, Lavi E, Weiss S R, Paterson Y
机构信息
Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia 19104-6076, USA.
出版信息
J Neurovirol. 2002 Jun;8(3):257-64. doi: 10.1080/13550280290049697.
Abstract
Murine hepatitis virus A59 infection of the central nervous system (CNS) results in CNS demyelination in susceptible strains of mice. In infected B-cell-deficient mice, demyelination not only occurred but was also more severe than in parental C57BL/6 animals. This increase may be due to the persistence of virus in the CNS in the absence of B cells. In mice lacking antibody receptors or complement pathway activity, virus did not persist yet demyelination was similar to parental mice. In infected RAG1(-/-) mice, moderately sized, typical demyelinating lesions were identified. Therefore, demyelination can occur in the absence of B and T cells.
摘要
小鼠肝炎病毒A59感染中枢神经系统（CNS）会导致易感品系小鼠出现中枢神经系统脱髓鞘。在感染的B细胞缺陷小鼠中，不仅发生了脱髓鞘，而且比亲代C57BL/6动物更为严重。这种增加可能是由于在没有B细胞的情况下病毒在中枢神经系统中持续存在。在缺乏抗体受体或补体途径活性的小鼠中，病毒不会持续存在，但脱髓鞘情况与亲代小鼠相似。在感染的RAG1（-/-）小鼠中，发现了中等大小的典型脱髓鞘病变。因此，在没有B细胞和T细胞的情况下也会发生脱髓鞘。
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