Hepatitis D pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Varun Kumar, M.B.B.S. [2]; João André Alves Silva, M.D. [3] Jolanta Marszalek, M.D. [4]
Overview
Pathogenesis
Life Cycle
To replicate efficiently, a virus requires the cooperation of the host cell at all stages of the replicative cycle:
- Attachment
- Penetration
- Uncoating
- Provision of appropriate metabolic conditions for the synthesis of viral macromolecules
- Final assembly of viral subunits
- Release of new virions
HDV also requires the presence of a helper hepadnavirus to provide the protein components for its own envelope. How HDV enters hepatocytes is still not known, but it may involve the interaction between HBsAg-L and a cellular receptor. The incoming HDV RNA is then transported into the nucleus, probably by the small form of delta antigen, HDAg-S. Binding of HDAg to RNA also protects the HDV RNAs from degradation.
Transmission
The routes of transmission of hepatitis D are similar to those for hepatitis B. Infection is largely restricted to persons at high risk of hepatitis B infection, particularly injecting drug users and persons receiving clotting factor concentrates.
Transmission is similar to that of HBV:
- Bloodborne and sexual
- Percutaneous (IV drug use, haemophiliacs)
- Permucosal (sexual)
- Perinatal (rare)
HDV is transmitted percutaneously or sexually through contact with infected blood or blood products.
Blood is potentially infectious during all phases of active hepatitis D infection. Peak infectivity probably occurs just before the onset of acute disease.
Associated Conditions
Macroscopic Pathology
Microscopic Pathology
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