Selected article for: "cell binding and JHM CoV strain"

Author: KYUWA, Shigeru; SUGIURA, Yuki
Title: Role of cytotoxic T lymphocytes and interferon-γ in coronavirus infection: Lessons from murine coronavirus infections in mice
  • Cord-id: rx2284lm
  • Document date: 2020_8_5
  • ID: rx2284lm
    Snippet: 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 c
    Document: 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).

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