A dedicated specimen (i.e. no other tests to be performed) is required for this assay.
Do not use heparin tubes
All micro collects MUST be EDTA.
Do not freeze unseparated PPT tubes . If the specimen requires freezing, the supernatant must be removed from the gel first.
Require a dedicated PPT tube specimen (no other tests requested).
Centrifuge PPT tube within 24 hours of collection.
Transport at 2 - 8 degrees C if transport time from collection is less than 72 hours. Transport frozen if more than 72 hours.
PCR
The assay for the detection of HDV RNA involves reverse transcription of genomic RNA followed by a one-tube, nested PCR specific for HDV sequences.
Hepatitis D virus infection is present worldwide and affects all age groups. Geographical distribution parallels that of hepatitis B, thus prevalence is highest in parts of Africa, South America, Romania, Russia, the Asia-Pacific region and the Mediterranean region including Southern Italy. Since the 1970's and 1980's, prevalence has declined significantly in Europe. Infection in the Asia-Pacific region includes high prevalence in Vietnam and certain of the pacific islands, notably Kiribati, Niue, Nauru and Western Samoa. Infection is rare in Fiji and in NZ Maori.
Hepatitis D virus (HDV) is a replication defective ssRNA virus. It has an absolute requirement for hepatitis B virus (HBV) helper function for the production of infectious virus. To be infectious, the mature HDV must be encapsulated in an entirely HBV derived outer envelope consisting of all three forms of HBV surface antigen. The internal nucleocapsid structure is composed of the viral RNA genome plus about 60 copies of delta antigen, the only HDV-encoded protein.
HDV can either infect simultaneously with HBV (co-infection) or infect an individual who is already an HBV carrier (superinfection).
Coinfection of HBV and HDV results in both acute HBV hepatitis and acute HDV hepatitis. Coinfection is usually acute and self-limiting with less than 5% resulting in chronic HDV.
Superinfection generally causes a severe acute hepatitis with a short incubation time that leads to chronic type D hepatitis in up to 80% of cases.
Fulminant hepatitis is rare but still about 10 times more common in hepatitis D than in other types of viral hepatitis. Mortality reaches 80%.
Chronic viral hepatitis D will progress to cirrhosis in about 60 to 70% of patients. Development of cirrhosis usually takes 5-10 years but it can appear as soon as 2 years after infection. Chronic hepatitis D may also lead to the development of hepatocellular carcinoma.
Control of HDV infection relies on control of HBV. With an effective HBV vaccine, global prevalence of HDV is declining.
References
1. WHO/CDS/CSR/EDC/2001.12. Word Health Organization. Department of Communicable Disease Surveillance and Response. Hepatitis Delta.
2. Abbas Z, Jafri W, Raza S. Hepatitis D: Scenario in the Asia-Pacific region. World Journal of Gastroenterology. 2010;16(5): 554-562.
3. Dimitrakakis M, Crowe S, Gust I. Prevalence of Delta Infection in the Western Pacific Region. Journal of Medical Virology.1986;18:335-339.
For further information contact the laboratory (contact via Lablink: 22000 or (09) 307-8995 or 0800 522 7587) ,or:
the Virology team
virology@adhb.govt.nz