Hepatitis D




Hepatitis D virus (HDV) is an RNA virus that is structurally unrelated to hepatitis A, hepatitis B, or hepatitis C virus. It was discovered in 1977. HDV causes a unique infection that requires the assistance of viral particles from hepatitis B virus (HBV) to replicate and infect other hepatocytes. Its clinical course is varied and ranges from acute, self-limited infection to acute, fulminant liver failure. Chronic liver infection can lead to end-stage liver disease and associated complications.


When a person becomes infected with the hepatitis D virus (HDV), the virus begins to multiply within the liver. Fourteen days to 180 days later, a person may develop hepatitis D symptoms.

However, not everyone infected with the hepatitis D virus will actually have symptoms. Also, some of the people who do develop symptoms will have only very mild symptoms. You can look and feel perfectly healthy, yet still be infected with the disease and infect others.

For a person with hepatitis D, symptoms (especially early symptoms) may include one or several of the following:

- Fatigue

- Excessive tiredness

- Not feeling very hungry

- Nausea or vomiting

- Diarrhea

- A low-grade fever

- Muscle pain

- Joint pain

- Sore throat

- Mild abdominal pain (or stomach pain)

- Dark urine

- Light-colored stool.

Often, these early symptoms may be confused with those commonly seen with the stomach flu.

Jaundice (yellowing of the skin or the whites of the eyes) usually occurs several days after early symptoms of hepatitis D first appear. However, it may occur up to two weeks after symptoms begin. At this point, early symptoms tend to improve; but other new symptoms, such as abdominal pain (or stomach pain) on the right side, may appear.


Hepatitis D is caused by the hepatitis delta virus (HDV), a defective RNA virus. HDV requires the help of a hepadnavirus like hepatitis B virus (HBV) for its own replication.

The routes of transmission of hepatitis D (HDV) are similar to those for hepatitis B(HBV). Infection is largely restricted to persons at high risk of hepatitis B infection, particularly injecting drug users and persons receiving clotting factor concentrates. HDV is transmitted through percutaneous or mucosal contact with infectious blood and can be acquired either as a coinfection with HBV or as superinfection in persons with HBV infection. 


Since HDV is dependent on HBV for replication, control of HDV infection is achieved by targeting HBV infections. All measures aimed at preventing the transmission of HBV will prevent the transmission of hepatitis D.

There is no vaccine for hepatitis D, but it can be prevented in persons who are not already HBV-infected by hepatitis B vaccination. HBV vaccination is therefore recommended to avoid HBV-HDV coinfection. However, HBV vaccination does not protect HBV carriers from infection by HDV and prevention of HBV-HDV superinfection can only be achieved through education to reduce risk behaviors (e.g. injecting drugs, tattooing).


Hepatitis D should be considered in any individual who is HBsAg positive or has evidence of recent HBV infection.

The diagnosis of acute hepatitis D is made after evaluation of serologic tests for the virus. Total anti-HDV are detected by commercially available radioimmunoassay (RIA) or enzyme immunoassay (EIA) kits.


Each of the markers of HDV infection, including IgM and IgG antibodies, disappears within months after recovery. In contrast, in chronic hepatitis D, HDV RNA, HDAg, and IgM and IgG anti-HD antibodies persist.





Currently there is no effective antiviral therapy available for treatment of acute or chronic type D hepatitis.

For infected patients, massive doses of a-interferon (9 million units three times a week for 12 months or 5 million units daily for up to 12 months) have yielded remissions, but most patients remained positive for HDV despite the improved disease conditions.

The effect of interferon is considered to be most likely an indirect one, possibly via an effect on the helper hepadnavirus and/or on the immune response to the infections.

Acyclovir, ribavirin, lamivudine and synthetic analogues of thymosin have proved ineffective.