Hepatitis D: The Most Severe Form of Viral Hepatitis
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Hepatitis D: The Most Severe Form of Viral Hepatitis
- 2. • Simultaneously infected with HBV • Severe chronic liver disease • Natural reservoir is man
- 3. In combination with hepatitis B virus, hepatitis D has the highest fatality rate of all the hepatitis infections, at 20%. It inhibits IFN-α Signalling.
- 7. Life Cycle
- 8. Delta Antigens • L-HDAg: later stage, inhibits viral replication, assembly • S-HDAg: early stage, supports viral replication
- 9. Transmission
- 10. Patterns of Infection • Co-infection: both HBV and HDV • Superinfection: HDV infection of an individual chronically infected with HBV. • HBV replication becomes suppressed during acute phase of HDV infection
- 12. Diagnosis • Anti-HD antibodies IgM and IgG • Immunohistochemical staining for HDAg • Serum HDV RNA • ELISA, PCR, molecular hybridization
- 14. Treatment and Prevention • The vaccine for hepatitis B protects against hepatitis D virus • Interferon alpha can be effective in reducing the severity of the infection (20% cases) • Can use pegylated form • The drug myrcludex B is in clinical trials as of October 2015
- 15. Thank you
Editor's Notes
- In addition to chronic liver disease, it can cause acute hepatitis, cirrhosis and hepatocellular carcinoma. It can be experimentally transmitted to chimpanzees.
- Regardless of the fact that HDV needs HBV for its life cycle, the distribution pattern of each virus is different. Genotype 1 is most common in Mongolia.
- The HDV is a small, spherical virus with a 36 nm diameter. It has an outer coat containing three HBV envelope proteins (called large, medium, and small hepatitis B surface antigens), and host lipids surrounding an inner nucleocapsid. The nucleocapsid contains single-stranded, circular RNA. There are 8 genotypes.
- Like Hepatitis B, HDV gains entry into liver cells via the sodium/bile co-transporter protein. After entering the hepatocyte, the virus is uncoated and the nucleocapsid translocates to the nucleus due to a signal. Since the nucleocapsid does not contain an RNA polymerase to replicate the virus’ genome, the virus makes use of the cellular RNA polymerases. Three forms of RNA are made; genomic RNA, antigenomic RNA, and a linear polyadenylated antigenomic RNA, which is the mRNA containing the open reading frame for the HDAg. HDV RNA is synthesized first as linear RNA that contains many copies of the genome. The genomic and antigenomic RNA contain a sequence of ribozyme, which self-cleaves the linear RNA into monomers. These monomers are then ligated to form circular RNA.
- HDV is known to produce one protein, namely HDAg. It comes in two forms; large-HDAg, and a small-HDAg. The N-terminals of the two forms are identical, they differ by 19 more amino acids in the C-terminal of the large HDAg. HDAg-S is produced in the early stages of an infection and enters the nucleus and supports viral replication. HDAg-L, in contrast, is produced during the later stages of an infection, acts as an inhibitor of viral replication, and is required for assembly of viral particles.
- Parenteral transmission. HDV is transmitted percutaneously or sexually through contact with blood or blood products
- Three specific HDV markers are HDV RNA, HDAg and anti-HDV. Hepatitis D virus RNA can be detected in serum by either molecular hybridization or RT-PCR. As HDAg, serum anti-HDV IgM and IgG antibodies can be detected by ELISA or RIA. Acute HBV/HVD co-infection is highlighted by the presence of a high titre of IgM anti-HBc, antibodies that disappear in chronic HBV infection. It bears otherwise the same characteristics as acute HDV superinfection. HDAg appears early but also disappears quickly. The titre of anti-HD antibodies of the IgG class is very high in chronic patients and may help distinguishing current from past infections.
- HDV is considered eradicated when both HDV RNA in the serum and HDAg in the liver become persistently undetectable. Myrcludex B inhibits virus entry into hepatocytes. IFN alpha: 9 million units three times a week. HDV relapse is almost always observed after cessation of treatment. Pegylated form of INF alpha has a longer activity with better outcomes.