Gupta Arundhati, Li Renfeng, Shair Kathy, Gao Shou-Jiang
Cancer Virology Program, UPMC Hillman Cancer Center, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
J Med Virol. 2025 Sep;97(9):e70581. doi: 10.1002/jmv.70581.
Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV) are oncogenic human gammaherpesviruses (GHVs) associated with a broad spectrum of malignancies and chronic diseases. However, direct studies of these viruses in humans are limited by ethical constraints, technical challenges, and their strict species specificity. To overcome these barriers, researchers have developed surrogate models, with murine gammaherpesvirus 68 (MHV68) emerging as a tractable and widely utilized system. MHV68 shares key genetic and biological features with EBV and KSHV, providing critical insights into GHV pathogenesis, including viral latency, reactivation, immune evasion, and virus-host interactions. This review summarizes current cellular and animal models for GHV research, highlighting the advantages and limitations of MHV68 as a model for studying human GHVs. We explore mechanisms of viral gene function, immune modulation, and host responses, and discuss how these models have advanced our understanding of GHV-associated diseases. Improved model systems will be essential for guiding future experimental approaches and developing targeted therapies for GHV-driven malignancies and other related disorders.
爱泼斯坦-巴尔病毒(EBV)和卡波西肉瘤相关疱疹病毒(KSHV)是致癌性人类γ疱疹病毒(GHV),与多种恶性肿瘤和慢性疾病相关。然而,在人体中对这些病毒进行直接研究受到伦理限制、技术挑战及其严格的物种特异性的制约。为克服这些障碍,研究人员开发了替代模型,其中小鼠γ疱疹病毒68(MHV68)成为一种易于处理且被广泛应用的系统。MHV68与EBV和KSHV具有关键的遗传和生物学特征,为深入了解GHV发病机制提供了重要见解,包括病毒潜伏、再激活、免疫逃逸以及病毒与宿主的相互作用。本综述总结了当前用于GHV研究的细胞和动物模型,强调了MHV68作为研究人类GHV模型的优势和局限性。我们探讨了病毒基因功能、免疫调节和宿主反应的机制,并讨论了这些模型如何增进我们对GHV相关疾病的理解。改进的模型系统对于指导未来的实验方法以及开发针对GHV驱动的恶性肿瘤和其他相关疾病的靶向治疗至关重要。