Glucose‑regulated protein 78 is an antiviral against hepatitis A virus replication
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- Published online on: April 28, 2017 https://doi.org/10.3892/etm.2017.4407
- Pages: 3305-3308
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Copyright: © Jiang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
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.
