LATENCY IN HERPESVIRUS INFECTIONS OF CELLS AND TISSUES

细胞和组织的疱疹病毒感染的潜伏期

• 批准号: 3124278
• 负责人: JACK G STEVENS
• 金额: $ 39.09万
• 依托单位: UNIVERSITY OF CALIFORNIA LOS ANGELES
• 依托单位国家: 美国
• 财政年份: 1978
• 资助国家: 美国
• 起止时间: 1978-11-01 至 1990-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3124278
• 关键词: Alphaherpesvirinae; Marek's disease; antiviral antibody; autoimmune disorder; biological models; cellular immunity; density gradient ultracentrifugation; electron microscopy; electrophoresis; genetic library; genetic manipulation; genetic mapping; genetic transcription; histopathology; humoral immunity; immunization; immunofluorescence technique; immunosuppression; molecular cloning; myelin; myelinopathy; neurons; spinal ganglion; tissue /cell culture; virus DNA; virus antigen; virus classification; virus cytopathogenic effect; virus genetics; virus replication

A series of variants of HSV which have altered patterns of pathogenesis in experimental animal systems have been identified. Examples include: 1) HSV-I and II intertypic recombinants (RE6 and RS6) which are non-neurovirulent when injected into adult mouse brains. 2) A strain of HSV-I (KOS) which is nonvirulent in mice when injected in foot pads. 3) A revertant of a ts mutant of HSV-I (tsI) which is not temperature sensitive for replication in non-nervous tissues, but which does not reactivate from the latent state in spinal ganglia at 38.50C. In addition, the inability of HSV-I to invade mesoderm in the CAM of embryonic chicks is being investigated. In all cases, trivial explanations for the altered pathogenicity have been rigorously excluded. Data are presented demonstrating that pathogenesis can be rescued using DNA transfections of wild-type parental DNA restriction fragments (molecularly cloned) and intact variant virus DNA followed by selection in vivo. A combined collaborative study of the genes and gene products involved in these and related examples of HSV pathology and neurovirulence using techniques of both molecular biology and pathobiology is described.

HSV 的一系列变种改变了发病机制的模式 实验动物系统已经确定。 示例包括：1) HSV-I 和 II 型间重组体（RE6 和 RS6） 注射到成年小鼠大脑中时无神经毒性。 2) 应变 HSV-I (KOS) 注射到小鼠足垫中时对小鼠无毒力。 3）A HSV-I (tsI) ts 突变体的回复体，对温度不敏感 用于在非神经组织中复制，但不会从 脊神经节的潜伏状态为 38.5 0 C。 此外，无能力 HSV-I 侵入胚胎鸡 CAM 中的中胚层的研究 调查了。 在所有情况下，对改变的简单解释 已严格排除致病性。 数据呈现 证明可以使用 DNA 转染来挽救发病机制 野生型亲本 DNA 限制片段（分子克隆）和 完整的变异病毒DNA，然后进行体内选择。 一个组合 参与这些的基因和基因产物的合作研究 使用以下技术进行 HSV 病理学和神经毒力的相关示例 描述了分子生物学和病理学。