Occurs sporadically and in epidemics in developing countries causing significant complications and death rates.
The fifth known form of human viral hepatitis.
Probably most common cause of acute hepatitis and jaundice in the world.
Global case fatality rate estimated to range from 0.2%-4%.
Mortality in pregnant women can be as high as 10-25%.
One third of the world’s population seropositive.
Hepatitis E virus, is a single-stranded RNA genome.
Replicates in the cytoplasm.
There are four genotypes of HEV and fall into two major groups: genotypes 1 and 2 are human viruses that cause epidemic hepatitis and associated with waterborne and fecal oral transmission, and genotypes 3 and 4 which are swine viruses that infect humans as an accidental host.
Viremia arises during the incubation period and antibodies, both IgG and IgM appear at the time of clinical onset and just preceding elevations in serum aminotransferase levels and symptoms.
Recovery is marked by viral clearance, increased IgG tigers, and decreasing IgM levels.
HEV is also present in stool during the incubation period, throughout active infection, and in the initial part of the recovery period.
The duration of viral shedding is variable, as is the presence of antibodies.
IgM anti-HEV antibodies remain detectable for 3 to 12 months, whereas IgG anti-HEV antibodies persist for years, if not for life.
In India the lifetime risk is more than 60%.
Usually a self-limited disease.
Clinically indistinguishable from other types of viral hepatitis.
Average incubation period is approximately 40 days.
Highest attack rates are among those 15-40 years.
Case fatality estimated to be 1-3%, with greater degree of severity with advancing age.
Pregnancy associated with the highest risk of liver failure with a mortality rate of 5-25%, and a high spontaneous abortion and stillbirth rate among survivors.
Nonenveloped single strand, positive sense RNA hepevirus.
4 genotypes: type 1 causes most human disease.
Hepatitis E virus genotype 3 causes self-limiting infection in non immunocompromised patients.
It can, however, lead to chronic hepatitis and cirrhosis in patients who are receiving immunologic suppression for solid organ transplants, who have HIV infection, and who have hematologic cancers and are receiving chemotherapy.
HEV in solid organ transplant recipients can evolve into chronic infection in approximately 66% of patients and to cirrhosis in10%.
In transplant patients infected with HEV several extrahepatic manifestation such as neurologic symptoms and kidney abnormalities have been reported.
Reduction of immunosuppressive therapy that targets T cells in patients with solid organ transplant and HEV infection, results in clearance of the virus in nearly 30% of such patients.
In patients who have received solid organ transplant and who had HEV infection monotherapy with ribavirin over three months resulted in sustained viral response and 78% of patients (Kamar N et al).