KSHV Abortive Replication Following De Novo Infection

从头感染后 KSHV 复制失败

• 批准号: 8541136
• 负责人: YAN YUAN
• 金额: $ 34.92万
• 依托单位: UNIVERSITY OF PENNSYLVANIA
• 依托单位国家: 美国
• 财政年份: 2013
• 资助国家: 美国
• 起止时间: 2013-05-08 至 2018-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8541136
• 关键词: Acquired Immunodeficiency Syndrome; Address; B-Lymphocytes; Cells; Chromosomes; DNA biosynthesis; Disease; Event; Exhibits; Family; Gur; Herpesviridae; Herpesviridae Infections; Human; Human Herpesvirus 4; Human Herpesvirus 8; In Vitro; Individual; Infection; Instruction; Investigation; Lead; Life Cycle Stages; Lytic; Malignant Neoplasms; Mediating; Multicentric Angiofollicular Lymphoid Hyperplasia; Nature; Nuclear Protein; Open Reading Frames; Pathogenicity; Peripheral Blood Mononuclear Cell; Process; Recombinants; Regulation; Repression; Research; Research Proposals; Role; Satellite Viruses; Simplexvirus; Staging; System; Testing; Viral; Viral Genome; Viral Pathogenesis; Viral Regulatory Proteins; Virion; Virus; in vivo; infected B cell; insight; latent infection; lytic replication; particle; primary effusion lymphoma; recombinant virus; role model; viral DNA

PROJECT SUMMARY (See instructions): KSHV infects B lymphocytes and establishes a predominantly latent infection. The detailed process and the mechanism underlying the establishment of latent infection remain elusive. After a KSHV particle enters a host cell, the virus undergoes D N A replication which results in accumulation of the viral genome to 50-100 copies per cell prior to establishment of latency. Little is known regarding the mode of the abortive viral replication and the regulation mechanism. ORF K8 encodes a nuclear protein of the bZip family. Gur study using K8-null recombinant virus demonstrated a role of KS in initial viral DNA replication following de novo KSHV Infection. K8-null viruses exhibit much lower viral genome copy numbers in comparison to wild type viruses when infecting 293T, HFF and HMVEC cells. The role of K8 in the early stage of de novo infection provides insights into the so-called

项目总结（见说明）： KSHV感染B淋巴细胞并建立主要的潜伏感染。潜伏感染建立的详细过程和机制仍然难以捉摸。在KSHV颗粒进入宿主细胞后，病毒经历DNA复制，这导致病毒基因组在潜伏期建立之前积累到每个细胞50-100个拷贝。关于病毒复制失败的模式和调控机制知之甚少。ORF K8编码bZip家族的核蛋白。Gur使用K8-null重组病毒的研究证明了KS在KSHV从头感染后的初始病毒DNA复制中的作用。当感染293 T、HFF和HMVEC细胞时，与野生型病毒相比，K8无效病毒表现出低得多的病毒基因组拷贝数。K8在新生感染早期阶段的作用提供了对所谓的