The epidemiological characteristics of hepatitis E virus are similar to those of hepatitis A, transmitted via the fecal-oral route, with distinct seasonality, often occurring during the rainy season or after floods. It does not become chronic and has a favorable prognosis.

bubble_chart Epidemiology

In 1989, Reyes et al. applied molecular cloning techniques to obtain a gene clone of the virus. In September 1989, it was officially named Hepatitis E Virus (HEV) and Hepatitis E (HE) at the International Hepatitis Conference in Tokyo. This disease is primarily found in some developing countries in Asia and Africa. In developed countries, it generally occurs as sporadic cases, while in developing countries, it tends to be epidemic. After 1980, there were several outbreaks in the Xinjiang region of China, and sporadic cases of Hepatitis E have been reported in other areas, accounting for about 10% of acute sporadic hepatitis. At least six provinces, municipalities, and autonomous regions have reported outbreaks of Hepatitis E. Its epidemic characteristics resemble those of Hepatitis A, being transmitted via the fecal-oral route. Waterborne outbreaks are the most common, with a few cases being foodborne outbreaks or transmitted through daily contact. It exhibits a distinct seasonality, often occurring after the rainy season or floods. The affected population is mainly young adults, with fewer cases among children and the elderly. Pregnant women are more susceptible, experiencing severe symptoms and a high mortality rate. There is no family clustering phenomenon, and the duration of outbreaks varies. The disease does not become chronic and has a good prognosis.

This type of HEV is orally transmitted, invades the liver through the intestines to replicate, and is excreted in feces during the late incubation period and the initial stage of illness.

bubble_chart Pathogen

Hepatitis E virus (HEV) is a single-stranded positive-sense RNA virus, currently classified under the genus Calicivirus. Virus-like particles observed using immune electron microscopy (IEM) techniques vary across reports from different regions, indicating sequence differences in HEV. However, these viral particles exhibit significant cross-reactivity, suggesting that HEV may have only one serotype. The virus is spherical, non-enveloped, with a diameter of 32–34 nm, and displays surface structures such as protrusions and indentations. Both solid and hollow particles can be observed, with the solid particles representing complete HEV and the hollow ones lacking the full genome. HEV primarily replicates in hepatocytes. It has been demonstrated that monkeys, cynomolgus macaques, African green monkeys, rhesus macaques, and chimpanzees are susceptible to HEV, and experimental infections in animals have been successful. In China, extracts from the feces of hepatitis E patients in Xinjiang and Shenyang were used to infect domestic macaques, successfully passing the infection through three generations. Animal experiments confirmed that HEV can be detected in bile before ALT levels rise and persists until ALT returns to normal. Polymerase chain reaction (PCR) testing of infected animals showed that HEV-RNA clearance in blood occurs almost simultaneously with that in feces. Enzyme-linked immunosorbent assay (ELISA) detection of anti-HEV antibodies in experimentally infected animals revealed seroconversion 2–6 weeks post-infection, peaking at 3–4 weeks, and declining to low levels after 6 weeks.

The pathological changes of this type of hepatitis resemble those of hepatitis A, including ballooning degeneration of hepatocytes, spotty or focal necrosis, and inflammatory cell infiltration in the portal area, primarily lymphocytes and mononuclear macrophages. There is evident bile stasis. Electron microscopy observations suggest that the liver cell damage in this disease may be related to a T-cell-mediated immune response.

bubble_chart Clinical Manifestations

The incubation period is 10 to 60 days, with an average of 40 days. According to three domestic epidemiological surveys on hepatitis E, the incubation period ranges from 15 to 75 days, averaging 36 days. Adults infected often exhibit clinical symptoms, while children show subclinical manifestations. The clinical symptoms and liver function impairment are more severe. Generally, it presents as a subclinical type. The clinical symptoms and liver function impairment are more severe. The onset is usually acute, with jaundice being common. Half of the cases experience fever, accompanied by weakness, nausea, vomiting, and liver pain. About one-third have arthralgia. Signs of cholestasis, such as cutaneous pruritus and light-colored stools, are more pronounced than in hepatitis A. Most patients exhibit hepatomegaly, while splenomegaly is less common. In most cases, jaundice subsides within about two weeks, and the course of the disease lasts 6 to 8 weeks, generally not progressing to chronicity. Pregnant women infected with HEV experience more severe conditions and are prone to liver failure, especially in the advanced stages of pregnancy, with a high fatality rate (10–39%). Late abortion and dead fetus may occur, possibly due to low serum immunoglobulin levels.

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bubble_chart Auxiliary Examination

Specific serological etiological examination is the basis for diagnosis.

1. Enzyme-linked immunosorbent assay (ELISA) detects anti-HEV IgM in serum, which is an indicator for the diagnosis of acute hepatitis E. Recombinant or synthetic polypeptides are used as antigens. In China, this method was used to test 111 cases of acute hepatitis E, with an anti-HEV positive rate of 86.5%. Among 32 patients in the convalescent stage, the anti-HEV positive rate was 6.3%, indicating that anti-HEV persists for a short time, with 63% turning negative 5–6 months after the illness.

2. Western Blot (WB) is more sensitive and specific than the ELISA method, but the operation is more complex and the detection time is longer.

3. Polymerase Chain Reaction (PCR) is used to detect HEV-RNA in the serum and feces of hepatitis E patients. This method has high sensitivity and strong specificity, but it is prone to laboratory contamination during operation, leading to false positives.

4. Immunoelectron microscopy (IEM) and immunofluorescence (IF) are used to detect HEV particles and HEV antigen (HEAg) in the feces, gallbladder, and liver tissues of hepatitis E patients. However, both methods require special equipment and techniques, and HEV exists for a short time in liver tissues, gallbladder, and feces, with a low positive rate, making them unsuitable for routine examination.

bubble_chart Diagnosis

The diagnosis should be based on clinical characteristics and liver function tests, with reference to epidemiological data, while excluding infections caused by HAV, HBV, HCV, and other causes of acute liver damage.

bubble_chart Treatment Measures

Proper rest and reasonable nutrition are the main focus, with selective use of medication as a supplement. Alcohol should be avoided, overexertion prevented, and hepatotoxic drugs avoided. Medication should be kept simple rather than complex.

1. Strict bed rest in the early stage is most important. Activity can be gradually increased as symptoms significantly improve, with the principle of not feeling fatigued. Treatment continues until symptoms disappear, the isolation period ends, and liver function returns to normal before discharge. After 1–3 months of rest, work can be gradually resumed.

2. The diet should suit the patient’s taste and consist of easily digestible, light foods. It should include multiple vitamins, sufficient calories, and an appropriate amount of protein, with fat not overly restricted.

3. For those with reduced food intake or vomiting, an intravenous drip of 10% glucose solution (1000–1500ml) with 3g vitamin C, 400mg glucurolactone, and 8–16U regular insulin can be administered once daily. Energy mixtures and 10% potassium chloride may also be added. For severe heat, modified *Yinchen Stomach Poria Decoction* can be used; for combined dampness-heat, modified *Yinchenhao Decoction* and *Weiling Decoction*; for liver qi depression, *Peripatetic Powder*; and for spleen deficiency with dampness retention, *Stomach-Calming Powder*. Some advocate using a high dose of *Red Peony Root* for deep jaundice, which can be effective. Generally, acute hepatitis can be cured.

bubble_chart Prevention

Similar to hepatitis A, the primary approach involves comprehensive measures focused on interrupting transmission routes. To prevent waterborne transmission, protecting water sources and managing fecal contamination are key. Attention to food hygiene, improving sanitation facilities, and maintaining personal hygiene are also crucial. Most reports indicate that using gamma globulin, common bletilla tuber, or human placental immunoglobulin is ineffective in preventing hepatitis E. Ultimately, the solution depends on vaccines, and the successful molecular cloning of HEV provides a foundation for vaccine development.