Book Cataloging CIP Data

III. Hepatitis D HD

Chapter 17

The earliest form of hepatitis D was a subtype of hepatitis B, though it was not yet officially named “hepatitis D.” In 1977, Rizzef et al. used immunoelectron microscopy to detect a new antigen in the nuclei of liver ce

From Book Cataloging CIP Data · Read time 1 min · Updated March 22, 2026

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  1. III. Hepatitis D (HD)

III. Hepatitis D (HD)

The earliest form of hepatitis D was a subtype of hepatitis B, though it was not yet officially named “hepatitis D.” In 1977, Rizzef et al. used immunoelectron microscopy to detect a new antigen in the nuclei of liver cells from Italian CHB patients—this antigen was named the 6 antigen or 6 factor. In 1980, it was discovered that the 6 factor isolated from laboratories possessed a complete viral particle structure. By 1984, international consensus recognized this as an independent pathogenic factor unrelated to hepatitis B, which was designated HDV (hepatitis D virus). HDV is a defective virus that requires assistance from hepatotropic viruses such as HBV to achieve replication and infection. The viral particles lack a nucleus or shell, with a diameter ranging from 35 to 37 nanometers. HDV (hepatitis D) typically cannot infect individuals on its own; its transmission relies on the assistance of HBsAg. Therefore, in areas where hepatitis B is prevalent, hepatitis D also becomes endemic. Although hepatitis D is relatively rare in China, with an infection rate of 1.6%–10%, small-scale outbreaks have occurred in Inner Mongolia, Xinjiang, and southwestern regions. The incubation period for hepatitis D is estimated to be 4–20 weeks. Since most cases of hepatitis D occur in conjunction with hepatitis B infections, known as co-infections, the clinical manifestations of hepatitis D are identical to those of hepatitis B, including loss of appetite, abdominal distension, chills and fever, jaundice, and pain in the liver region. However, hepatitis D tends to have a more acute onset than simple hepatitis B, with more severe liver damage and a relatively poorer prognosis, often leading to chronicity and a higher mortality rate. In summary, HDV can exacerbate liver cell damage; when hepatitis B patients become co-infected with HDV, in addition to the more severe disease itself, the condition is more likely to progress to LC or HCC.

The diagnosis of hepatitis D primarily relies on detecting anti-HDV antibodies or HDV RNA. Treatment is similar to that for hepatitis B, focusing on liver protection and supportive care. Interferon therapy has shown some efficacy, though the cure rate remains only 10%–15%, and the treatment is expensive. Traditional Chinese medicine and herbal remedies remain the preferred options at present, as hepatitis D has never been epidemic in Gansu Province; only sporadic cases have been reported, and experience is still limited. However, the principles, methods, formulas, and medications used in treating hepatitis D are largely consistent with the diagnostic and therapeutic approaches for hepatitis B.

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