1. Division of Viral Hepatitis
Epidemiology and Prevention of Viral Hepatitis A to E: Hepatitis D (Delta) Virus
[SLIDE 1] Title Slide
This slide set presents an overview of the clinical and epidemiologic features for viral hepatitis A, B, C, D, and E and prevention measures for these infections. More detailed information regarding the epidemiologic features and prevention measures can be found on-line at for hepatitis A read the MMWR, Prevention of Hepatitis A Through Active or Passive Immunization: Recommendations of the Advisory Committee on Immunization Practices, Vol. 48, No RR12;1, 10/01/1999; for hepatitis B read the MMWR, Recommendations to Prevent Hepatitis B Virus Transmission – US, Vol.44, No 30;574, 08/04/1995, Updated; for hepatitis C read the MMWR, Recommendations for Prevention and Control of Hepatitis C Virus (HCV) Infection and HCV-Related Chronic Disease, Vol. 47, No RR19;1, 10/16/1998.
Division of Viral Hepatitis

2. Hepatitis D (Delta) Virus
HBsAg
RNA
d antigen
[SLIDE 65] Hepatitis D (Delta) Virus
HDV is a defective single‑stranded RNA virus that requires the helper function of HBV to replicate. HDV requires HBV for synthesis of envelope protein composed of HBsAg, which is used to encapsulate the HDV genome.

3. Geographic Distribution of HDV Infection
Taiwan
Pacific Islands
[SLIDE 70] 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 among 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 in parts of Russia and Romania, the prevalence of HDV infection is very high among both asymptomatic HBV carriers (>20%) and among 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 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.)
Low
HDV Prevalence
High
Intermediate
Very Low
No Data

4. Hepatitis D - Clinical Features
Coinfection with HBV
severe acute disease
low risk of chronic infection
Superinfection on top of chronic HBV
usually develop chronic HDV infection
high risk of severe chronic liver disease 20 20 20

5. Typical Serological Course
HBV – HDV Coinfection
Typical Serological Course
Time after Exposure
Anti-HBs
Symptoms
ALT Elevated
Total anti-HDV
IgM anti-HDV
HDV RNA
HBsAg
Titer
[SLIDE 68] HBV‑HDV Coinfection: Typical 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 subdetectable 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.

6. HBV – HDV Super-infection Typical Serological Course
Jaundice
Symptoms
ALT
Total anti-HDV
IgM anti-HDV
HDV RNA
HBsAg
Titer
Time after Exposure
[SLIDE 69] HBV‑HDV Superinfection: Typical Serologic Course
In patients with chronic HBV infection who are superinfected with HDV several characteristic serologic features generally occur, including:
the titer of HBsAg declines at the time HDAg appears in the serum,
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,
high titers of both IgM and IgG anti‑HDV are detectable, which persist indefinitely

7. Percutanous exposures
Hepatitis D Virus
Modes of Transmission
Percutanous exposures
injecting drug use
Permucosal exposures
sex contact 21 21 21

8. HBV-HDV Superinfection
Hepatitis D - Prevention
HBV-HDV Coinfection
Pre or postexposure prophylaxis to prevent HBV infection (HBIG and/or Hepatitis B vaccine)
HBV-HDV Superinfection
Education to reduce risk behaviors among persons with chronic HBV infection 25 25 25