A Baskiran1, A Atay2, D Y Baskiran3, S Akbulut1. 1. Department of General Surgery, Faculty of Medicine, Inonu University Turgut Ozal Medical Center, Institute of Liver Transplantation, Malatya, Turkey. 2. Department of General Surgery, Izmir Katip Celebi University Atatürk Training and Research Hospital, Izmir, Turkey. atayarif@hotmail.com. 3. Department of Public Health, Faculty of Medicine, Inonu University Turgut Ozal Medical Center, Malatya, Turkey.
Abstract
AIM: Given the current literature data, this article aims to shed light on the epidemiological and clinical effects of HBV, as well as its impact on the development of hepatocellular carcinoma (HCC). METHODS: A review of the English language literature based on a MEDLINE (PubMed) database was searched. The keywords were cirrhosis, hepatocellular carcinoma, epidemiology, hepatitis delta virus, hepatitis B virus, and co-infection. All references from retrieved papers were reviewed systematically to find additional collection of reports. RESULTS: The study has broadly confirmed the contribution of HDV viremia to liver disease and cirrhosis. However, uncertainty over the mechanism of action on HCC development remains. As the recent data has demonstrated, the HCC-HDV has a unique molecular profile which is distinct from that of HBV-HCC. CONCLUSION: Owing to the dependence of HDV on HBV, it is not clear whether HCC is a consequence of the cumulative effect of both HBV and HDV, an effect of the underlying cirrhosis, or a direct oncogenic effect of HDV. Many questions concerning the oncogenic role of HDV remain unanswered. To better understand the role of HDV in carcinogenesis, studies at the molecular level that consider genotype differences should be increased. Multicenter, high-volume, and prospective studies that compare HBV/HDV co-infected and HBV-infected individuals will be pivotal in determining the oncogenic role of HDV.
AIM: Given the current literature data, this article aims to shed light on the epidemiological and clinical effects of HBV, as well as its impact on the development of hepatocellular carcinoma (HCC). METHODS: A review of the English language literature based on a MEDLINE (PubMed) database was searched. The keywords were cirrhosis, hepatocellular carcinoma, epidemiology, hepatitis delta virus, hepatitis B virus, and co-infection. All references from retrieved papers were reviewed systematically to find additional collection of reports. RESULTS: The study has broadly confirmed the contribution of HDV viremia to liver disease and cirrhosis. However, uncertainty over the mechanism of action on HCC development remains. As the recent data has demonstrated, the HCC-HDV has a unique molecular profile which is distinct from that of HBV-HCC. CONCLUSION: Owing to the dependence of HDV on HBV, it is not clear whether HCC is a consequence of the cumulative effect of both HBV and HDV, an effect of the underlying cirrhosis, or a direct oncogenic effect of HDV. Many questions concerning the oncogenic role of HDV remain unanswered. To better understand the role of HDV in carcinogenesis, studies at the molecular level that consider genotype differences should be increased. Multicenter, high-volume, and prospective studies that compare HBV/HDV co-infected and HBV-infected individuals will be pivotal in determining the oncogenic role of HDV.