Department of Molecular Genetics and Microbiology, UF Health Cancer Center, College of Medicine, University of Florida, Gainesville, Florida 32610, USA.
HIV and AIDS Malignancy Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892, USA; email:
Annu Rev Virol. 2021 Sep 29;8(1):349-371. doi: 10.1146/annurev-virology-011921-082615.
Gammaherpesviruses are an important class of oncogenic pathogens that are exquisitely evolved to their respective hosts. As such, the human gammaherpesviruses Epstein-Barr virus (EBV) and Kaposi sarcoma herpesvirus (KSHV) do not naturally infect nonhuman primates or rodents. There is a clear need to fully explore mechanisms of gammaherpesvirus pathogenesis, host control, and immune evasion in the host. A gammaherpesvirus pathogen isolated from murid rodents was first reported in 1980; 40 years later, murine gammaherpesvirus 68 (MHV68, MuHV-4, γHV68) infection of laboratory mice is a well-established pathogenesis system recognized for its utility in applying state-of-the-art approaches to investigate virus-host interactions ranging from the whole host to the individual cell. Here, we highlight recent advancements in our understanding of the processes by which MHV68 colonizes the host and drives disease. Lessons that inform KSHV and EBV pathogenesis and provide future avenues for novel interventions against infection and virus-associated cancers are emphasized.
γ疱疹病毒是一类重要的致癌病原体，它们经过高度进化以适应各自的宿主。因此，人类γ疱疹病毒 EBV（Epstein-Barr 病毒）和 KSHV（卡波济肉瘤相关疱疹病毒）不会自然感染非灵长类动物或啮齿动物。非常有必要充分探索宿主中γ疱疹病毒发病机制、宿主控制和免疫逃逸的机制。1980 年首次报道了一种从鼠科啮齿动物中分离出的γ疱疹病毒病原体；40 年后，实验室小鼠感染鼠γ疱疹病毒 68（MHV68、MuHV-4、γHV68）已成为一种成熟的发病机制系统，其可用于应用最先进的方法来研究从宿主整体到单个细胞的病毒-宿主相互作用。在这里，我们重点介绍了我们对 MHV68 定植宿主并引发疾病的过程的理解的最新进展。强调了对 KSHV 和 EBV 发病机制有启示作用的经验教训，并为针对感染和病毒相关癌症的新型干预措施提供了未来的途径。
