Glucose-regulated protein 78 is an antiviral against hepatitis A virus replication

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 stu...

Descripción completa

Detalles Bibliográficos
Autores principales: Jiang, Xia, Kanda, Tatsuo, Haga, Yuki, Sasaki, Reina, Nakamura, Masato, Wu, Shuang, Nakamoto, Shingo, Shirasawa, Hiroshi, Okamoto, Hiroaki, Yokosuka, Osamu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Articles
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5450597/
https://www.ncbi.nlm.nih.gov/pubmed/28587404
http://dx.doi.org/10.3892/etm.2017.4407
Descripción
Sumario: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.

Ejemplares similares