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犬瘟热病毒引起中枢神经系统感染:血脑屏障的破坏及抗病毒抗体的促进作用

Establishment of central nervous system infection by canine distemper virus: breach of the blood-brain barrier and facilitation by antiviral antibody.

作者信息

Krakowka S, Cork L C, Winkelstein J A, Axthelm M K

机构信息

Department of Veterinary Pathobiology, College of Veterinary Medicine, Ohio State University, Columbus 43210.

出版信息

Vet Immunol Immunopathol. 1987 Dec;17(1-4):471-82. doi: 10.1016/0165-2427(87)90163-2.

DOI:10.1016/0165-2427(87)90163-2
PMID:2963430
Abstract

Morphologic, immunologic and virologic data implicating antiviral antibody in promoting entry of canine distemper virus (CDV) into brain and reticuloendothelial tissues are reviewed. Infection of central nervous system (CNS) endothelium precedes invasion of virus-positive and -negative leukocytes into Virchow-Robin spaces and central nervous system (CNS) parenchyma by 1-3 days. Platelets are implicated in initiation of endothelial infection in that: CDV-infected dogs are thrombocytopenic; platelets from CDV-infected dogs contain IgG-virus complexes on their plasma membranes; platelet microthrombi were observed adjacent to foci of endothelial infection, and; CDV-susceptible ferrets rendered thrombocytopenic by antiplatelet antibody exhibit delayed viral entry into CNS tissues. Renal glomerular-bound IgG, IgM and occasionally CDV antigen were demonstrated in CDV-infected dogs by immunocytochemical techniques. Distemper-infected dogs with inherited C3 deficiency exhibited enhanced renal glomerular disease associated chiefly with deposition of IgM in mesengial regions vs. their homozygous normal CDV-infected littermates. Direct infusion of virus-positive leukocytes, plasma and platelets into the CNS capillary bed via the right carotid artery should establish the primacy of each in the initiation of CNS vascular endothelial infection by CDV.

摘要

本文综述了形态学、免疫学和病毒学数据,这些数据表明抗病毒抗体在促进犬瘟热病毒(CDV)进入脑和网状内皮组织中发挥作用。中枢神经系统(CNS)内皮细胞感染先于病毒阳性和阴性白细胞侵入Virchow-Robin间隙和中枢神经系统(CNS)实质1-3天。血小板与内皮细胞感染的起始有关,具体表现为:感染CDV的犬出现血小板减少;感染CDV的犬的血小板质膜上含有IgG-病毒复合物;在内皮细胞感染灶附近观察到血小板微血栓,并且;通过抗血小板抗体使血小板减少的对CDV易感的雪貂,病毒进入CNS组织的时间延迟。通过免疫细胞化学技术在感染CDV的犬中检测到肾肾小球结合的IgG、IgM以及偶尔的CDV抗原。与同基因正常感染CDV的同窝仔犬相比,患有遗传性C3缺乏症的感染犬瘟热的犬表现出更严重的肾小球疾病,主要与系膜区域IgM沉积有关。通过右颈动脉将病毒阳性白细胞、血浆和血小板直接注入CNS毛细血管床,应能确定它们各自在CDV引发CNS血管内皮感染中的首要作用。

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