Hepatitis E is a viral hepatitis (liver inflammation) caused by infection with a virus called hepatitis E virus (HEV). It is one of five known human hepatitis viruses: A, B, C, D, and E. HEV is a positive-sense single-stranded RNA icosahedral virus with a 7.5 kilobase genome. HEV has a fecal-oral transmission route. Infection with this virus was first documented in 1955 during an outbreak in New Delhi, India.
The incubation period of hepatitis E varies from 3 to 8 weeks. After a short prodromal phase symptoms lasting from days to weeks follow. They may include jaundice, fatigue and nausea. The symptomatic phase coincides with elevated hepatic aminotransferase levels.
Viral RNA becomes detectable in stool and blood serum during incubation period. Serum IgM and IgG antibodies against HEV appear just before onset of clinical symptoms. Recovery leads to virus clearance from the blood, while the virus may persist in stool for much longer. Recovery is also marked by disappearance of IgM antibodies and increase of levels of IgG antibodies.
While usually an acute disease, in immunocompromised subjects- particularly in solid organ transplanted patients- hepatitis E may cause a chronic infection. Occasionally this may cause liver fibrosis and cirrhosis.
Infection with a virus called hepatitis E virus (HEV).
Improving sanitation is the most important measure in prevention of hepatitis E; this consists of proper treatment and disposal of human waste, higher standards for public water supplies, improved personal hygiene procedures and sanitary food preparation. Thus, prevention strategies of this disease are similar to those of many others that plague developing nations, and they require large-scale international financing of water supply and water treatment projects.
A vaccine based on recombinant viral proteins was developed in the 1990s and tested in a high-risk population (military personnel of Nepal) in 2001. The vaccine appeared to be effective and safe, but development was stopped for economic reasons, since hepatitis E is rare in developed countries. There is no licensed hepatitis E vaccine for use in the US.
Although other HEV vaccine trials, including trials conducted in populations in southern Asia, have shown candidate vaccines to be effective and well-tolerated, these vaccines have not yet been produced or made available to susceptible populations. The exception is China. After more than a year of scrutiny and inspection by China's State Food and Drug Administration (SFDA), a hepatitis E vaccine developed by Chinese scientists was available at the end of 2012. This vaccine-called HEV 239 and sold as Hecolin by its developer Xiamen Innovax Biotech-was approved for prevention of hepatitis E in 2012 by the Chinese Ministry of Science and Technology, following a phase 3 trial on two groups of 50,000 people each from Jiangsu Province where none of the vaccinated became infected during a 12-month period, compared to 15 in the group given placebo treatment. The first vaccine batches came out of Innovax' factory in late October 2012, and will be sold to Chinese distributors.
The commonly used tests for HEV infection include detection of IgM and IgG anti-HEV antibodies and detection of HEV RNA. IgM anti-HEV antibodies can be detected during the first few months after HEV infection, whereas IgG anti-HEV antibodies represent either recent or remote exposure. The presence of HEV RNA indicates current infection, whether acute or chronic.
Hepatitis E does not become chronic, and people do not become carriers.
Apart from supportive care, no specific validated treatment exists for acute hepatis E infection. Although ribavirin is not registered for Hepatitis E treatment, there is off-label experience for treating chronic Hepatitis E with this compound. The use of low doses, 600 to 800 milligrams per day, of ribavirin over a three-month period has been associated with viral clearance in about two-thirds of chronic cases. Other possible treatments include peginterferon or a combination of ribavirin and peginterferon. In general chronic HEV infection is associated with immunosuppressive therapies, but remarkably little is known about how different immunosuppressants affect HEV infection. In one thirds of patients with solid-organ transplantation viral clearance can be achieved by temporal reduction of the level of immunosuppression.