单纯疱疹病毒I型（HSV1）在感染宿主细胞的过程中，由于细胞内的防御反应导致对病毒基因组DNA的异染色质化，对此，病毒编码的蛋白分子随之通过与细胞内某些蛋白分子的相互作用，使被此染色质化静默了的基因组DNA开始进入转录启动阶段。我们前期制备的病毒衣被蛋白UL7基因突变毒株的分析表明，该蛋白控制病毒增殖及其对动物的致病能力的表型特征依赖于其与细胞组蛋白及其表观修饰酶的相互作用，并以此参与了细胞核内病毒的染色质化基因组DNA的重聚/解构过程，对该线索的进一步分析，将基于其不同突变体形式与不同的细胞蛋白分子和病毒编码分子的相互作用，深化对HSV1基因组DNA通过染色质重聚/解构模式及其随后的转录启动及相关调控这一复杂机理的认识，在此基础上，探讨比较HSV1在溶胞性感染和潜伏感染过程中其基因组的转录调控功能，深入理解这个病毒感染人体后的潜伏感染及其病理过程的分子生物学机理。

In the course of herpes simplex virus type 1 (HSV 1) infection in host cells, cellular defense reaction is identified to lead to heterochromatization of viral genome DNA, which thereby makes the viral encoding protein molecules initiating the transcription of silenced genome DNA by chromatin remodeling via interaction with some cellular protein molecules. As shown in the previous analysis of recombinant viral strain with tegument protein UL7 gene mutation, the phenotype characterization of controlling viral proliferation and its correlated weaker pathogenicity of UL 7 protein in animals largely depends upon its interactions with cellular histones and epigenetic modification enzymes, and subsequently involves in the remodeling of chromatized viral genome DNA in nucleus. Prior to the primary analysis, to explore the interaction of individual mutational viral strains with different cellular protein molecules and viral encoding molecules would be facilitating further understanding of the complicated mechanism of initiating the transcription and associated regulation of HSV1 genome DNA via the chromatin remodeling pattern, and then to compare the transcriptional regulation functions of HSV1 genome in the course of either lytic or latent infection, as well as to further recognize the molecular biology mechanism of HSV1 latent infection and its pathologic progress upon infection of human body.