KSHV Abortive Replication Following De Novo Infection

项目总结(见说明)： KSHV感染B淋巴细胞并建立一种主要的潜伏感染。建立潜伏感染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D NA复制，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。关于病毒复制流产的方式和调控机制，我们知之甚少。ORF K8编码bZip家族的核蛋白。用K8缺失重组病毒进行的GUR研究表明，KS在新生KSHV感染后的初始病毒DNA复制中起到了作用。当K8缺失病毒感染293T、HFF和HMVEC细胞时，与野生型病毒相比，病毒基因组拷贝数要低得多。K8在新发感染早期阶段的作用为我们提供了对所谓

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