Hepatitis D

The following information is from the Hepatitis Resources Center of the National Center for Infectious Diseases.

Hepatitis D (Delta) Virus (HDV) is a defective single-stranded RNA virus that requires the helper function of Hepatitis B virus (HBV) to replicate. HDV requires HBV for synthesis of envelope protein composed of HbsAg (hepatitis B surface antigen), which is used to encapsulate the HDV genome.

Clinical Features

HDV infection is acquired either as a coinfection with HBV or a superinfection of persons with chronic HBV infection. Persons with HBV-HDV coinfection may have more severe acute disease and a higher risk of hepatitis with rapid liver failure (2% to 20%) compared to those infected with HBV alone; however, chronic HBV infection appears to occur less frequently in persons with HBV-HDV coinfection. Chronic HBV carriers who acquire HDV superinfection usually develop chronic HDV infection. In long-term studies of chronic HBV carriers with HDV superinfection, 70%-80% have developed evidence of chronic liver diseases with cirrhosis compared with 15%-30% of patients with chronic HBV infection alone.
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Transmission

The modes of HDV transmission are similar to those for HBV, with percutaneous exposures the most common. Sexual transmission of HDV is less efficient common than with HBV. Perinatal HDV transmission is rare.
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Coinfection with Hepatitis B and D

Typical Blood Tests (Serologic Course): The serologic course of HDV infection varies depending on whether the virus is acquired as a coinfection with HBV or as a superinfection of a person with chronic HBV infection. In most persons with HBV-HDV coinfection, both IgM antibody to HDV (anti-HDV) and IgG anti-HDV are detectable during the course of infection. However, in about 15% of patients, the only evidence of HDV infection may be the detection of either IgM anti-HDV alone during the early acute period of illness or IgG anti-HDV alone during convalescence. Anti-HDV generally declines to undetectable levels after the infection resolves and there is no serologic marker that persists to indicate that the patient was ever infected with HDV.

Hepatitis Delta antigen (HDAg) can be detected in serum in only about 25% of patients with HBV-HDV coinfection. When HDAg is detectable, it generally disappears as HBsAg disappears and most patients do not develop chronic infection. Tests for IgG anti-HDV are commercially available in the United States. Tests for IgM anti-HDV, HDAg and HDV RNA by PCR are only available in research laboratories.
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Supercoinfection with Hepatitis B and D

Typical Serologic Course: In patients with chronic HBV infection who are superinfected with HDV, several characteristic serologic features generally occur, including:

1. The concentration of HBsAg declines at the time HDAg appears in the serum;
2. HDAg and HDV RNA remain detectable in the serum because chronic HDV infection generally occurs in most patients with HDV superinfection, unlike the case with coinfection;
3. High concentration of both IgM and IgG anti-HDV are detectable, which persist indefinitely.
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Geographic Distribution of HDV Infection

In general, the global pattern of HDV infection corresponds to the prevalence of chronic HBV infection; however, several distinct features of the distribution of HDV infection have been identified. In countries with a low prevalence of chronic HBV infection, HDV prevalence is generally low among both asymptomatic HBV carriers (<10%) and patients with chronic HBV-related liver disease (<25%). HDV infection in these countries occurs most commonly among injecting drug users and persons with hemophilia. In countries with moderate and high levels of chronic HBV prevalence, the prevalence of HDV infection is highly variable.

In southern Italy and parts of Russia and Romania, the prevalence of HDV infection is very high among both asymptomatic HBV carriers (>20%) and patients with HBV-related chronic liver disease HBV (>60%). Other countries, including northern Italy, Spain, Turkey and Egypt, have a moderate prevalence of HDV infection among asymptomatic HBV carriers (10%-19%) and among patients with chronic HBV-related liver disease (30%-50%). However, in most of Southeast Asia and China, where the prevalence of chronic HBV infection is very high, HDV infection is uncommon. In some South American countries situated in the Amazon River Basin, periodic epidemics of HDV infection have occurred among chronic HBV carriers in relatively isolated regions. Disease related to HDV infection in these outbreaks has been very severe, with rapid progression to fulminant hepatitis and case-fatality rates of 10%-20%. The cause of the atypical course of HDV infection in these populations is unknown.

*Note: The map of anti-HDV prevalence generalizes available data and patterns may vary within countries.
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Prevention

Because HDV is dependent on HBV for replication, HBV-HDV coinfection can be prevented with either pre- or post-exposure prophylaxis for HBV. However, no products exist to prevent HDV superinfection of persons with chronic HBV infection. Thus, prevention of HDV superinfection depends primarily on education to reduce risk behaviors.



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