Kyuwa Shigeru, Sugiura Yuki
Laboratory of Biomedical Science, Department of Veterinary Medical Science, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyou-ku, Tokyo 113-8657, Japan.
J Vet Med Sci. 2020 Oct 20;82(10):1410-1414. doi: 10.1292/jvms.20-0313. Epub 2020 Aug 5.
Murine coronavirus (CoV) is a beta-CoV that infects mice by binding to carcinoembryonic antigen-related cell adhesion molecule 1. Intraperitoneal infection with the murine CoV strain JHM (JHMV) induces acute mild hepatitis in mice. While both innate and acquired immune responses play a significant role in the protection against murine CoV infection in mice, CD8 cytotoxic T lymphocytes (CTLs) and interferon-γ are essential for viral clearance in JHMV-induced hepatitis. In addition, CoVs are characterized by high diversity, caused by mutations, recombination, and gene gain/loss. 25V16G is an immune-escape JHMV variant, which lacks a dominant CTL epitope. By evading immune responses, 25V16G establishes persistent infections, leading to granulomatous serositis in interferon-γ-deficient mice. These examples of CoV-associated pathogenesis in mice might provide useful information on other CoV infections, including coronavirus disease 2019 (COVID-19).
鼠冠状病毒(CoV)是一种β冠状病毒,通过与癌胚抗原相关细胞粘附分子1结合来感染小鼠。用鼠冠状病毒株JHM(JHMV)进行腹腔感染可在小鼠中诱发急性轻度肝炎。虽然先天免疫和获得性免疫反应在小鼠抵抗鼠冠状病毒感染的过程中都发挥着重要作用,但CD8细胞毒性T淋巴细胞(CTL)和干扰素-γ对于JHMV诱导的肝炎中的病毒清除至关重要。此外,冠状病毒的特点是具有高度多样性,这是由突变、重组以及基因获得/缺失引起的。25V16G是一种免疫逃逸的JHMV变体,它缺乏一个显性CTL表位。通过逃避免疫反应,25V16G建立持续性感染,导致干扰素-γ缺陷小鼠出现肉芽肿性浆膜炎。小鼠中这些与冠状病毒相关的发病机制实例可能会为包括2019冠状病毒病(COVID-19)在内的其他冠状病毒感染提供有用信息。