Hepatitis D virus (HDV)
Deltavirus (tentative) genus
Negative sense single strand circular RNA virus
Transmitted through blood, via body fluid, sexual
contact, or transplacentally → travels in blood to hepatocytes → infects cells
→ replicates and released only from those cells also infected with HBV, because
it requires hepatitis B surface antigen (HBsAg) to form an infectious particle
(HDV is defective/non-infectious and cannot replicate alone)
you must have an active hepatitis B infection to get a hepatitis D
infection. This can either be achieved
by co-infection or sequential infection (B then D).
Viral antigens on infected hepatocytes
recognized by host immune response → CTL activated → inflammation, hepatocyte
necrosis → hepatitis more severe than with HBV alone
Those at greatest risk are IV drug users.
Hepatitis D is endemic to the Mediterranean
Delta antigen detection
Anti-delta antigen IgM antibodies
D worsens the clinical symptoms
experienced with hepatitis B, both with the co-infection and superinfection.
This is primarily due to the fact that the hepatitis D virus is directly
cytotoxic to hepatocytes.
Coinfection: higher chance of liver
failure and quicker progression to cirrhosis.
Superinfection: often results in severe
acute hepatitis in a patient already chronically infected with HBV.
(controls HBV infection, which limits HDV infection)
recombinant Hepatitis B Surface Antigen to prevent HBV infection
rid of HBV guarantees elimination of HDV
HBV carriers who become superinfected with HDV
have a much poorer prognosis, with a greater chance of fulminant hepatitis and
HDV may also have a cytopathic effect
independent of a host immune response.
The HDV genome is a ribozyme, which is an RNA
particle able to cleave and ligate itself. No other human viruses behave this
way, but many plant viruses in the viroid group do.
- Avoid exposure (blood products, IVDU, sexual)
- Prevent / treat Hepatis B