期刊
EXPERIMENTAL AND THERAPEUTIC MEDICINE
卷 13, 期 6, 页码 3305-3308出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2017.4407
关键词
CRISPR/Cas9; endoplasmic reticulum stress; glucose-regulated protein 78; hepatitis A virus
资金
- Ministry of Health, Labour and Welfare of Japan
- Research Program on Hepatitis from the Japan Agency for Medical Research and Development (AMED)
Infection with hepatitis A virus (HAV) is a major cause of acute hepatitis globally and it is important to identify the mechanisms of HAV replication. Glucose-regulated protein 78 (GRP78) is an endoplasmic reticulum (ER) chaperone and serves a role in unfolded protein response pathways. Previous studies have demonstrated that GRP78 functions as an endogenous antiviral factor. In the present study, two loss-of-function studies using GRP78 were completed to elucidate the role of GRP78 in HAV infection. HAV replication was observed to be enhanced by deficient GRP78 although GRP78-deficiency also led to lower expression of ER stress molecules downstream of GRP78. Therefore, GRP78 appears to be a potential novel defensive molecule against HAV in hepatocytes.
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