Hepatitis E is caused by infection with hepatitis E virus (HEV). Hepatitis E is a waterborne disease and contaminated water or food supplies from a single source can lead to major outbreaks in developing countries.

HEV causes acute sporadic and epidemic viral hepatitis. Symptomatic HEV infection is most common in adults aged 15-40 years. Occasionally, a severe form of hepatitis develops, with mortality rates ranging between 0.5% - 4.0% of the overall population. This severe form of hepatitis may reach a mortality rate of 20% during pregnancy in the 3rd trimester.

Recent seroprevalence studies indicate high prevalence of HEV infection among healthy populations in some industrial countries with historically low occurrence of Hepatitis E including the US, Japan and Europe.

EARLY DIAGNOSIS OF HEPATITIS E

Early detection of HEV antibodies is very important for the efficient treatment and prevention of the spread of the disease.IgM is one of the most reliable markers for acute infection. Although indirect-ELISA assays for detection of HEV IgM are available, they are not applicable for routine diagnosis because of the low sensitivity and specificity and high rate of false negative results.With most of the currenty commerciay avaialbe assays, the detection of IgG precedes the detected seroconversion of IgM.

Our approach in developing of HEV immunoassays relies on optimizations in the detection techniques and improvements in the quality of antigens and antibodies which we use.

We utilize a recombinant capsid antigen (E2) expressed from the highly conserved region of ORF2 of the HEV. This antigen expresses some important conformation antigenic epitopes of the native virus and shows extremely high reactivity to HEV specific antibodies. With this antigen, we have significantly improved the sensitivity and specificity of our HEV assays.

We have developed four different types of HEV ELISA tests that have multiple applications and can be easily adapted for both clinical diagnosis and scientific research. HEV-IgM ELISA is intended for early diagnosis of patients suspected for infection with HEV

The hypothesis that HEV infection is a zoonosis was supported with accumulating evidence. Swine HEV and later an avian HEV have been identified and sequenced separately in 1997 and  2001. HEV infection induces production of anti-HEV antibodies and includes viremia and feces excretion of HEV. Consumption of uncooked deer meat infected with HEV has led to acute hepatitis E in humans in Japan. Also in Japan, reports for HEV genome sequences detected in pig livers sold in supermarkets which supports the hypothesis for the wide spread of HEV among pigs in many parts of the world.

The current estimation is that over 90% of the pigs among pig farms in UK, Holland, the US,etc is infected with HEV.

While HEV transmission usually occurs by eating and drinking contaminated food and water, blood transfusion is another route of infection.

In China, HEV seroprevalence of the general population is about 40% and increases with age at a rate of about 1% per year. Acute infection, as estimated by the prevalence of IgM anti-HEV and the spontaneous rise of IgG anti-HEV levels, occurs at about 4% per year. Asymptomatic viremia has been estimated to be approximately 0.3%. 

In a study conducted with 44,816 donor samples were collected in China from 2002 to 2008, the HEV seroprevalences of blood donors ranged from 29.9% to 41.7% with rates of acute HEV infection ranged from 0.43% to 1.51%. The rates of viremia among the donors in 6 different regions of China ranged from 0.02% to 0.14%. These results also showed a high prevalence of viremia among anti-HEV IgM-positive samples.  A total of 7.14% (30/420) of anti-HEV IgM-positive samples were RNA positive, but none of the IgM-negative samples were HEV RNA positive.