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World J Gastroenterol. Oct 28, 2014; 20(40): 14589-14597
Published online Oct 28, 2014. doi: 10.3748/wjg.v20.i40.14589
Hepatitis D virus infection, replication and cross-talk with the hepatitis B virus
Chi-Ruei Huang, Szecheng John Lo
Chi-Ruei Huang, Szecheng John Lo, Institute of Microbiology and Immunology, National Yang-Ming University, Taipei 112, Taiwan
Chi-Ruei Huang, Szecheng John Lo, Department and Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan 333, Taiwan
Szecheng John Lo, Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan 333, Taiwan
Author contributions: Huang CR and Lo SJ both wrote the main text of this review article.
Supported by Grants (CMRPD-1C0811) from Chang Gung Memorial Hospital, the National Science Council and the National Health Research Institute to Lo SJ
Correspondence to: Szecheng John Lo, PhD, Department of Biomedical Sciences, College of Medicine, Chang Gung University, 259 Wen-Hwa 1st Road, Taoyuan 333, Taiwan. losj@mail.cgu.edu.tw
Telephone: +886-3-2118800-3295 Fax: +886-3-2118392
Received: October 28, 2013
Revised: May 12, 2014
Accepted: June 20, 2014
Published online: October 28, 2014
Core Tip

Core tip: Hepatitis D virus (HDV) is a defective virus that depends on hepatitis B virus (HBV) to supply envelope proteins (HBsAgs) for assembling a new virion. The association of the clinical severity of hepatitis with HDV genotypes (HDV-1 to 8) has been reported, but the mechanism is unknown. Whether the combinations of HBV genotypes (A to H) with HDV genotypes cause varying clinical outcomes remains to be explored. This review focuses on HDV replication, the cross-talk between HDV and HBV, and the endoplasmic reticulum (ER) stress induced by HBsAgs in the ER which results in the promotion of large delta antigen export from the nucleus to interact with HBsAgs.