Consensus has not been reached regarding the complete pathogenesis of HEV.  Evidence shows that the virus exposes its RNA within the host cell's cytoplasm, where it is translated into a negative RNA strand that contains ORFs 1, 2 and 3 that are involved in the replication of the virus.  HEV is not cytopathic, and the manifestations of the disease result from the body's immune response towards the infected cells.  The transmission of the disease depends on the genotype of the virus.  It may be transmitted through ingestion of contaminated water, in genotypes 1 and 2, or ingestion of uncooked meat, genotypes 3 and 4.  Acute hepatitis E has been noted to progress to chronic disease in HIV infected patients with a low CD4 count.  Solid organ transplanted patients are commonly asymptomatic, or have mild symptoms of the disease.  60% of infected patients with an organ transplant, develop chronic hepatitis E, and 10% develop liver cirrhosis.  Infection is usually due to HEV genotype 3, and diagnostic studies should be based on the identification of HEV RNA by PCR technique.  Histological changes of the liver of patients with chronic disease include: portal hepatitis; lymphocytic infiltrates; necrosis; and  fibrosis.
Hepatitis E pathophysiology
Hepatitis C pathophysiology
Hepatitis B pathophysiology
Autoimmune hepatitis pathophysiology
Alcoholic hepatitis pathophysiology
Primary biliary cirrhosis pathophysiology
Peliosis hepatis pathophysiology
Primary sclerosing cholangitis pathophysiology