The innate immune responses triggering production of type I interferons and inflammatory cytokines constitute a nonspecific innate resistance that eliminates invading pathogens including viruses. The activation of innate immune signaling through pattern recognition receptors (PRRs) is by sensing pathogen-associated molecular patterns derived from viruses. According to their distribution within cells, PRRs are classified into three types of receptors: membrane, cytoplasmic, and nuclear. Kaposi’s sarcoma-associated herpesvirus (KSHV), a large DNA virus, replicates in the nucleus. Its genome is protected by capsid proteins during transport in the cytosol. Multiple PRRs are involved in KSHV recognition. To successfully establish latent infection, KSHV has evolved to manipulate different aspects of the host antiviral innate immune responses. This review presents recent advances in our understanding about the activation of the innate immune signaling in response to infection of KSHV. It also reviews the evasion strategies used by KSHV to subvert host innate immune detection for establishing a persistent infection.

触发 I 型干扰素和炎性细胞因子产生的先天免疫反应构成了一种非特异性先天抗性，可消除包括病毒在内的入侵病原体。通过模式识别受体 (PRR) 激活先天免疫信号是通过检测源自病毒的病原体相关分子模式。根据它们在细胞内的分布，PRR 分为三种类型的受体：膜受体、细胞质受体和核受体。卡波氏肉瘤相关疱疹病毒 (KSHV) 是一种大型 DNA 病毒，在细胞核中复制。它的基因组在胞质溶胶中的运输过程中受到衣壳蛋白的保护。KSHV 识别涉及多个 PRR。为了成功建立潜伏感染，KSHV 已经进化到可以操纵宿主抗病毒先天免疫反应的不同方面。本综述介绍了我们对响应 KSHV 感染的先天免疫信号激活的理解的最新进展。它还回顾了 KSHV 用来破坏宿主先天免疫检测以建立持续感染的逃避策略。