Abstract

Hepatitis Delta is an inflammatory liver disease caused by the hepatitis Delta virus (HDV), a defective RNA virus that requires the mandatory helper function of hepatitis B virus (HBV) for its transmission and life cycle. For this reason, HDV is acquired either as a coinfection of the two viruses or as a superinfection of chronic HBV carriers. The clinical outcome is different: coinfection usually runs a self-limited course that terminates with the clearance of both viruses and complete recovery in most cases, due to a transient hepatitis B surface antigenemia, which is required to support HDV replication (Fig. 1). The clinical course and outcome of superinfection varies, but it generally causes severe acute hepatitis with a relatively short incubation period, leading to a progressive chronic hepatitis in over 90% of cases (Fig. 2). More than 350 million people in the world are considered to have chronic HBV infection, and about 5% of them have serological evidence of exposure to HDV, leading to a burden of at least 15-20 million HDV cases worldwide. The improvement in socioeconomic conditions and the introduction of vaccination programs against HBV have resulted in a significant decrease in the incidence of HDV infection over the past two decades, particularly in southern Europe. 1 However, the prevalence of HDV has risen to levels not seen since the late 1990s due to the immigration of persons from areas where HDV is still endemic, such as eastern Europe, the Middle East, central Africa, and northern South America. 2 The clinical scenario of chronic HDV infection has changed accordingly. The percentage of individuals with active cirrhosis due to chronic hepatitis Delta increased from 20% in the 1980s to almost 70% in the 1990s due to progressive disease in patients who survived the epidemics of the 1970s and 1980s. 3 As a consequence, the current

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