Journal
EXPERIMENTAL AND THERAPEUTIC MEDICINE
Volume 13, Issue 6, Pages 3305-3308Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2017.4407
Keywords
CRISPR/Cas9; endoplasmic reticulum stress; glucose-regulated protein 78; hepatitis A virus
Categories
Funding
- Ministry of Health, Labour and Welfare of Japan
- Research Program on Hepatitis from the Japan Agency for Medical Research and Development (AMED)
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available