Clinical Features

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Delta agent may be spread in semen, vaginal secretions and blood via transfusion, needlestick injury, and intravenous drug supplies. Transmission from mother to child is rare.



Subclinical or asymptomatic infection may result in up to 90% of patients infected with HDV. Non-specific presentation includes jaundice, fatigue, anorexia, nausea, vomiting, hepatic tenderness, and dark urine.



HDV genotypes (genotypes I, II, and III) affect clinical picture of HDV differently.

Infection with genotype I results in mild to severe hepatic disease and may be associated with liver cirrhosis and hepatoceullar carcinoma. (Enomoto) Many patients with genotype II infections are asymptomatic carriers or experience less severe hepatitis than infection of genotype I. Genotype III causes fulminant hepatitis, or acute liver failure in the absence of pre-existing liver disease.

General outcomes of HDV infection include: acute hepatitis, cirrhosis, fulminant hepatitis, and chronic HDV infection.

FIGURE Outcomes of HDV infection. Length of progression to disease denoted by arrow lengths. Super infection of HBV carrier causes more rapid, severe progression than co-infection (shorter arrow).



Co-infection occurs when a person becomes simultaneously infected with HBV and delta agent. HBV must first establish infection within the host before HDV can begin to replicate. HBV-HDV co-infection may increase the risk of fulminant hepatitis (2%-20%) and cause a more severe acute disease as compared with individuals infected with only HBV.

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Super infection

Super infection results from HDV infection of HBV carriers. An individual seropositive for HBV and subsequently infected with delta agent is at risk for a more rapid and severe hepatic disease progression and development of chronic hepatitis. Chronic liver disease results in 70%-80% of HBV seropositive patients who acquire HDV superinfection as compared to 15%-30% of patients with chronic HBV infection alone.

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