Caspase inhibitors block MHV-3 induced apoptosis and enhance viral replication and pathogenicity.
Caspase inhibitors block MHV-3 induced apoptosis and enhance viral replication and pathogenicity.
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Caspase 抑制剂可阻断 MHV-3 诱导的细胞凋亡并增强病毒复制和致病性。
DOI：
10.1007/978-1-4615-1325-4_17
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发表时间：
2001
影响因子：
--
通讯作者：
Belyavskaya,E
中科院分区：
文献类型：
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作者：
Leibowitz,JL;Belyavskaya,E
与在A/J小鼠中观察到的轻微疾病相比，感染小鼠肝炎病毒株3(MHV-3)会导致BALB/c小鼠发生致死性肝炎(Levy，Leibowitz和Edgington，1981)。巨噬细胞对MHV感染的反应是MHV诱导的肝炎结局的关键决定因素(Levy，Leibowitz和Edgington，1981；Shif和Bang，1969)。我们以前已经证明，感染MHV-3的A/J巨噬细胞会在大多数被感染的细胞中触发细胞凋亡(Belyavskyi等人，1998)。相比之下，感染BALB/c巨噬细胞只会导致一小部分细胞发生凋亡。在这份报告中，我们利用caspase抑制剂来研究这一假说，即A/J小鼠来源的巨噬细胞快速诱导凋亡限制了MHV的复制和MHV感染期间的肝损伤。
Infection with mouse hepatitis virus strain 3 (MHV-3) results in lethal hepatitis in BALB/c mice, compared to the minimal disease observed in A/J mice (Levy, Leibowitz, and Edgington, 1981). The response of the macrophage to MHV infection is a key determinant of the outcome of MHV-induced hepatitis (Levy, Leibowitz, and Edgington, 1981; Shif and Bang, 1969). We have previously shown that infection of A/J macrophages with MHV-3 triggers apoptosis in most of the infected cells (Belyavskyiet al., 1998). In contrast, infection of BALB/c macrophages results in only a small percentage of the cells undergoing apoptosis. In this report we have utilized caspase inhibitors to investigate the hypothesis that the rapid induction of apoptosis in macrophages derived from A/J mice limits MHV replication and hepatic injury during MHV infection.