Hepatitis D pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: ; Jolanta Marszalek, M.D. [2] João André Alves Silva, M.D. [3]
Overview
Pathogenesis
There has been much progress in the understanding of the pathogenesis of hepatitis delta virus(HDV), but the mechanisms determining whether a person will spontaneously clear HDV, become chronically infected, or rapidly progress to hepatic fibrosis are not yet fully understood.[1] Pathological changes in HDV are limited to the liver, the only organ in which HDV can replicate. Hepatitis delta angtigen (HDAg) is not directly cytotoxic to human hepatocytes, nor has viral load shown to be associated with severity of liver injury. HDV viremia has however, been associated with an increased level of ALT and supressed HBV in the acute phase. [1] HBV is an essential cofactor in the evolution of hepatocellular damage, and infection with both HBV and HDV leads to more severe liver injury than HBV infection alone. More data is necessary to further the understanding of underlying mechanisms of HDV-induced disease. The host immune response to the virus plays an important role in liver injury and clearance of the virus although both innate and adaptive immune responses are poorly defined.
Observational cohort studies have shown that during the acute phase of HDV infection, HDV viremia is associated with an increased level of alanine aminotransferase(ALT) and suppressed HBV. In the chronic phase, HDV RNA decreases, HBV reactivates, and levels of ALT are only moderately high.
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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References
- ↑ 1.0 1.1 Hughes SA, Wedemeyer H, Harrison PM (2011). "Hepatitis delta virus". Lancet. 378 (9785): 73–85. doi:10.1016/S0140-6736(10)61931-9. PMID 21511329.