Inquiry Basket
Loading ......
Hepatitis E is an acute infectious disease transmitted through fecal oral transmission. Since the first outbreak of hepatitis E caused by water pollution in India in 1955, it has been prevalent in India, Nepal, Sudan, and Kyrgyzstan in the Soviet Union. In September 1989, the Tokyo International HNANB and Hematological Infectious Diseases Conference officially named hepatitis E, and its pathogen, Hepatitis E Virus (HEV), belongs to the hepatitis E virus genus of the hepatitis E virus family in taxonomy.
Figure 1. Hepatitis E virus (HEV) genome and virion structure. (Shahini, Endrit, et al.2024)
HEV is a single stranded positive stranded RNA virus, spherical in shape, with a diameter of 27-34nm and no envelope. Its nucleocapsid is icosahedral and stereosymmetric. It is not yet possible to culture HEV in vitro, but chimpanzees, crab eating monkeys, rhesus monkeys, African green monkeys, and silk monkeys are sensitive to HEV and can be used for virus isolation.
HEV is stable in alkaline environments and can maintain its integrity in the presence of magnesium and manganese ions. It is sensitive to high heat and can be inactivated by boiling.
Figure 2. Hepatitis E virus (HEV) viral life cycle. (Shahini, Endrit, et al.2024)
The HEV gene is 7.6kb in length, with a poly A tail at the 3 'end and three open reading frames (ORFs):
The hepatitis E virus infects approximately 20 million people annually. In 2015, these caused approximately 3 million people to suffer from acute illnesses and 44000 deaths. Pregnant women are particularly susceptible to complications from HEV infection, and they may develop 30% or more fatal acute illnesses. HEV is the leading cause of disease and death in developing countries, and also a disproportionate cause of maternal mortality. Hepatitis E is prevalent in Central Asia, while outbreaks have also been reported in Central America and the Middle East. Hepatitis E is becoming increasingly prevalent in developed countries, with 848 cases of hepatitis E virus infection reported in England and Wales in 2015.
Hepatitis E virus (HEV) is an unencapsulated spherical particle. HEV is divided into 8 genotypes, ranging from 1 to 8. The predominant strain is type 1 (formerly known as the Myanmar strain), followed by type 4. HEV cannot be cultured in cells yet, but it can infect various monkey species such as macaques in the laboratory. HEV has weak resistance to the external environment.
The transmission route (mainly through fecal oral route) and clinical manifestations (latent infection and acute hepatitis, not causing chronic hepatitis, etc.) of hepatitis E are similar to those of hepatitis A. Hepatitis E is highly prevalent in young people and adults aged 15-39. Hepatitis E is also a self limiting disease. HEV also has no direct pathological effect on liver cells (CPE). The body can acquire a certain degree of immunity after illness, but it is not stable enough. There is a hepatitis E vaccine, and the prevention of hepatitis E mainly relies on cutting off the fecal oral transmission route.
Detection of serum anti HEV IgM and anti HEV IgG: EIA detection is used. Serum anti HEV IgG begins to be detected 7 days after onset, which is one of the characteristics of HEV infection.
Detection of HEV RNA in serum and feces: RT-PCR is commonly used to collect early onset specimens.
HEV is excreted with the patient's feces, transmitted through daily contact, and can cause outbreaks or outbreaks through contaminated food and water sources. The peak incidence is often during the rainy season or after floods. The incubation period is 2-11 weeks, with an average of 6 weeks. Most clinical patients have mild to moderate hepatitis, which is often self limiting and does not progress to chronic HEV. Mainly affecting young adults, more than 65% occur in the age group of 16-19 years old, and children have more subclinical manifestations of infection. The adult mortality rate is higher than that of hepatitis A, especially for pregnant women who suffer from severe hepatitis E, with a mortality rate of 20% in the last 3 months of pregnancy. After HEV infection, it can produce immune protection to prevent reinfection of the same or even different strains of HEV. It has been reported that the majority of patients have anti HEV antibodies in their serum that persist for 4-14 years after recovery. Experimental diagnosis can be achieved by using electron microscopy to detect virus particles in feces, RT-PCR to detect HEV-RNA in feces and bile, and ELISA to detect anti HEV IgM, IgG antibodies, etc. in serum using recombinant HEV glutathione S-transferase fusion protein as antigen. Hepatitis E is generally prevented in the same way as hepatitis B, and emergency passive immunization with regular immunoglobulin is ineffective.
| Host Genetic Factors | Details |
| Interferon Regulatory Factor 3 (IRF3) | A host transcription factor that activates IFN production in response to viral infection. Polymorphisms in IRF3 that reduce its activity are associated with increased susceptibility to severe HEV infection. |
| STAT3 | A key mediator of IFN signaling. Mutations in STAT3 impair the host's ability to clear the virus, increasing the risk of chronic infection. |
| Human Leukocyte Antigen (HLA) Genes | Certain HLA alleles are associated with enhanced immune responses to HEV, reducing disease severity, while others correlate with increased risk of severe hepatitis. |
At present, there is no drug that is safe and effective for hepatitis E, and there are no large-scale randomized clinical trials of antiviral drugs. A review of existing small-scale studies suggests that ribavirin can be considered effective for immunocompromised individuals with chronic infections. Chronic HEV infection is associated with immunosuppressive therapy, and when this occurs in solid organ transplant patients, reducing immunosuppressive drugs can lead to HEV clearance in one-third of patients.
Reference
| Target | Cat. No. | Product Name | Size | Applications | |
| HEV | DEIA076 | Total Antibody to Hepatitis E Virus, HEV-Ab ELISA Kit | 96T | Competitive ELISA | Inquiry |
| DEIA077 | Antigen to Hepatitis E Virus, HEV-Ag ELISA Kit | 96T | sELISA | Inquiry |
| Target | Cat. No. | Product Name | Host | |
| HEV | DAG-WT377 | Recombinant Hepatitis E Virus (HEV) VLP | HEK293 | Inquiry |
| HEV ORF2 | DAG3139 | Recombinant Hepatitis E Virus ORF2 Protein [GST] | E. coli | Inquiry |
| HEV ORF | DAG-WT536 | Recombinant Hepatitis E Virus ORF2 (a.a 1-660) [His] | HEK293 | Inquiry |
Loading ......
