HDV Genetic Variability and Clinical Patterns

The wide radiation of HDV we describe might contribute to the spectrum of pathologies associated with HDV. For example, specific liver lesions, including morula cells, have been observed in severe hepatitis in African and Amazonian patients (Casey et al. 1993; Parana et al. 1995). It is therefore considered that the association of HDV-3-HBV/F leads to severe acute hepatitis. By contrast HDV-2 and HDV-4 have been typically associated with less severe hepatitis disease than Type I-associated infections (Wu et al. 1995). However, a recent study among the Miyako island strains suggests that the HDV-4 Okinawa subgroup (labelled IIb-M in the original paper) induces a greater progression to chronic hepatitis and to cirrhosis (Watanabe et al. 2003). Type-I viruses have a wide spectrum of pathologies, ranging from severe fulminant hepatitis in Sweden (Hansson et al. 1982; Zhang and Hansson 1996), Russia (Flodgren et al. 2000) and Taiwan (Wu et al. 1995) to very mild disease in the town of Archangelos in the island of Rhodes (Hadziyannis et al. 1991) and in Mongolia (Inoue et al. 2005). All African samples studied in our work came from the screening of HDV replication markers in patients with liver disease who were immigrating into France. Most patients suffered from active chronic hepatitis or cirrhosis and some of them underwent liver transplantation. Although the delta viruses corresponding to the African radiation in this study are associated with severe liver-specific HDV histological lesions, it should be emphasized that these virus lineages might not necessarily be as pathogenic in the general population. Obviously, other factors such as the time and duration of infection, the viral load (Le Gal et al. 2005), the appearance of defective HDV RNA molecules (Wu et al. 2005), the HBV helper strain and the genetic background of the patient (Dieye et al. 1999) may contribute to the pathogenicity.

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