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Federico Costante,1,* Leonardo Stella,1,* Francesco Santopaolo,1,2 Antonio Gasbarrini,1,2 Maurizio Pompili,1,2 Tarik Asselah,3,* Francesca Romana Ponziani1,2 1Internal Medicine and Gastroenterology - Hepatology Unit, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, 00168, Italy; 2Department of Translational Medicine and Surgery, Catholic University, Rome, 00168, Italy; 3Service d’Hépatologie, Hôpital Beaujon UMR 1149 Inserm - Université de Paris, Clichy, France*These authors contributed equally to this workCorrespondence: Francesca Romana Ponziani; Federico Costante, Internal Medicine and Gastroenterology - Hepatology Unit, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Largo Francesco Vito 1, Rome, 00168, Italy, Tel +390630156264, Email francesca.ponziani@gmail.com; federico.costante93@gmail.comAbstract: Hepatitis D virus (HDV) infection affects more than 10 million people worldwide, with an estimated prevalence of nearly 4.5% among HBsAg-positive individuals. Epidemiological studies have shown a significant increase in the prevalence of hepatocellular carcinoma (HCC) in patients with chronic HDV infection compared to those with chronic hepatitis B virus (HBV) mono-infection. Despite the clinical findings, data on molecular oncogenic mechanisms are limited and fragmentary. Moreover, the role of HDV in promoting the development of HCC has so far been controversial, because it is difficult to weigh the respective contributions of the two viruses. In this review, we focused on the direct oncogenic action of HDV, its role in modifying the tumor microenvironment, and the genetic signature of HDV-related HCC, comparing these features with HBV-related HCC.Keywords: hepatitis B virus, hepatitis delta virus, chronic hepatitis B, CHB, chronic delta hepatitis, CDH, dual infection, HCC |
