中文摘要：

程序性细胞死亡因子-4（programmed celld eath-4，PDCD4）通过阻断相关基因的转录与翻译从而抑制肿瘤发生，单纯疱疹病毒-1（herpes simplex virus-1，HSV-1）US3蛋白激酶可有效调控病毒基因产物或外源因素引致的细胞凋亡。近期研究证明PDCD4在病毒感染细胞中以US3依赖及非依赖两种模式被磷酸化修饰，其中受US3修饰的PDCD4仍定位细胞核并随之被降解，这可能是细胞凋亡被抑制的主要原因之一，此外，PDCD4沉默可阻断复制不完全病毒引致的细胞凋亡，表明PDCD4与HSV-1 US3阻断细胞凋亡途径直接相关。本文综述了这两种蛋白及其作用关系的研究进展，为解析病毒与细胞相互作用机理提供新方向。

英文摘要：

Programmed cell death 4 （PDCD4） is a tumor suppressor factor that can inhibit tumorigenesis by suppressing transcription and translation of related genes. The US3 protein kinase of herpes simplex virus-1 （HSV-1） is sufficient to block apoptosis induced by viral gene products or exogenous agents. A recent report establishes a link between PDCD4 and US3, and presents that PDCD4 is involved in apoptosis which is blocked by HSV-1 US3. PDCD4 can be posttranslationally modified in infected cells both in a US3- dependent and -independent fashion. US3-dependent modification retains PDCD4 in infected cell nuclei and thus can be degraded via the ubiquitin pathway. This is probably the one of the main reasons for inhibition of apoptosis. Furthermore, PDCD4 depletion can block apoptosis induced by a replication-defective virus. This review describes recent advances in two proteins and their relationship, and improves our understanding of the interaction between virus and host cells.