卡波氏肉瘤相关疱疹病毒（KSHV）是一种人类疱疹病毒。KSHV潜伏感染基因表达模式的形成是病毒建立潜伏感染的基础。KSHV在感染细胞后，大量病毒基因表达迅速受到抑制，仅少量潜伏态相关基因表达以维持病毒基因组的有效复制。KSHV在感染细胞早期如何与宿主相互作用，实现大量病毒基因表达的沉默以及在潜伏感染基因表达模式形成后如何防止病毒再激活以维持长期潜伏感染，其机制尚未阐明。我们将利用KSHV内皮细胞感染模型，通过基因表达谱分析，探索KSHV潜伏感染早期的分子事件；同时将研究潜伏态相关核抗原（LANA）是否在病毒感染早期调控病毒基因组的表观遗传修饰；我们还将通过系统生物学的方法鉴定KSHV再激活过程中的宿主限制因子以及深入研究RTA-TLE2功能复合体在KSHV潜伏感染维持过程中的功能机制。通过上述工作，加深理解KSHV潜伏感染基因表达模式的调控,为KSHV感染及相关疾病的防治提供新的线索。

Kaposi's Sarcoma associated herpesvirus (KSHV) is the most recently identified human herpesvirus and tumor virus. The establishment and maintenance of KSHV latent genes expression pattern is essential for KSHV latent infection. After the infection of host cell, the expression of most KSHV genes are silenced, except for a few viral latent genes that support basic viral genome replication. It is not fully clarified how KSHV cooperates with the host factors to shut down viral genes expression at the early stage of its infection, and to prevents viral reactivation as to achive a persistent latency after the establishment of viral latent genes expression pattern. We will explore the early molecular events of KSHV infection by gene expression profiles; we will also demonstrate whether LANA regulates epigenetic codes of viral genome at the early stage of viral infection; In addition, we will identify the host restriction factors of KSHV reactivation by systematic methods and will contiune to study the functions of RTA-TLE2 complex in KSHV latency maintenance.Through these studies, we will reveal more details of the mechanisms by which KSHV regulates latent genes expression pattern and provide new insights for the therapy of KSHV infection and related disease.