classificationHEV belongs to the family Hepaviridae, genus Hepavirus, and genotype V. The Australian isolate is different from the American and Canadian isolates and belongs to a variant strain.

morphologyIt is a spherical, non enveloped, symmetrical virus particle with a diameter of 32-34nm. There are cup-shaped structures on the surface that resemble cup-shaped viruses.

chemical composition It is a single stranded positive stranded RNA molecule containing poly (A), with a total length of 6654bp except for the poly (A) tail, which is about 600bp shorter than HEV in humans and pigs. The avian HEV genome is separated by a 5 '- non coding region (NCR), followed by three partially overlapping open reading frames (ORFs) and 3' - NCRs. ORF1 is located at the 5 '- end of the genome and encodes a non structural protein. The polyprotein encoded by avian HEV ORF1 contains several putative functional domains, including methyltransferase, papain like cysteine protease, helicase, and chicken RNA polymerase. They are also present in mammalian HEVs, further supporting the conclusion that avian HEV is a member of the hepatitis virus genus.

The impact on physical and chemical factors:

Iodide small accumulation and high-pressure sterilization destroy the virus. Can survive in harsh environments. The transmission through fecal oral route indicates that avian HEV can resist the acidic and weak alkaline environment in the intestine without inactivation.

Intravenous inoculation of avian HEV can promote proliferation in chicken embryos, while other conventional methods of inoculation cannot promote proliferation. The transfection of RNA transcripts from avian HEV infectious eDNA clones into LMH chicken embryo cells has been demonstrated to support the replication of avian HEV.

Epidemiology:

HS syndrome was reported to occur in western Canada in 1991, and now it occurs in eastern Canada, California, and the Midwest and East of the United States. Australia has reported on BLS. Serological investigations indicate that there are also cases of avian HEV infection in the UK. Caged aircraft carrier class is susceptible, and HS syndrome frequently occurs on some farms. This disease has also been reported in laying hens, and sporadic deaths in laying hens and small groups of chickens raised on bedding may be related to it. HEV infection in poultry in the United States is endemic in chicken flocks. A serological survey of avian HEV antibodies was conducted on 1276 broiler chickens of different ages from 76 states, and it was found that 71% of chicken flocks and 31% of chickens in the United States tested positive for HEV antibodies. Young chickens (under 18 weeks old) aged 17 months and 36% of adult chickens aged 18 months are positive for HEV specific antibodies.

Under wild conditions, chickens are the host of avian HEV.

Transmission routeFecal oral infection indicates that the feces of infected chickens are the main source of the virus, and vertical transmission of HEV can occur in hens infected with HEV.

Clinical symptoms:

The incubation period from viral infection to excretion from feces in chickens with oral and nasal infections is 1-3 weeks. The incidence rate and mortality rate are relatively low, and the egg production rate of some explosive disease chickens has decreased by more than 20%, while some are not affected. The mortality rate of HS syndrome in laying broiler breeders and 30-72 week old laying hens is higher than that of normal, and the incidence rate of HS syndrome in 40-50 week old laying hens is higher. The mortality rate increases by approximately 0.3% per week during the mid-term of egg production, sometimes exceeding 1%. The clinical symptoms of BLS cases in Australia are also different. The affected chickens may have cockscomb, pale flesh, depression, loss of appetite, contamination of anal feathers, or pasty feces. Infected chicken flocks produce small eggs with thin shells and light colors, but the internal quality, fertilization rate, and hatching rate of the eggs are not affected. Cases in the United States and Canada exhibit milder symptoms or only subclinical infections.

Pathological changes:

Under natural conditions, dead chickens typically exhibit ovarian degeneration, red fluid in the abdomen, and enlarged liver and spleen. Infection before death and usually in good physical condition, accompanied by a disastrous loss of cockscomb and sagging, but sometimes the condition of the chicken can also be seen to be very poor. Hepatomegaly, bleeding or blood clots can be seen in the abdominal cavity. The liver usually becomes brittle, with colored spots and red, yellow, and/or yellow brown lesions, hematoma under the capsule, and blood clots attached to the surface. The occurrence of coagulation and liver bleeding in the abdominal cavity is often confused with hemorrhagic fatty liver syndrome (HFLS). HFLS usually occurs in laying hens, but hepatitis hemorrhagic syndrome (HS syndrome) does not result in hepatic steatosis.

The histological lesions of the liver range from multifocal bleeding to extensive necrosis, bleeding, and infiltration of heterophilic granulocytes and monocytic inflammatory cells around the hepatic veins. There is often partial lymphocyte infiltration and a few plasma cells around the portal vein. It is also common for similar eosinophilic substances such as amyloid to aggregate in the interstitial spaces of liver cells and to separate liver cells. In severe cases, granulomas with discontinuous portal vein can be seen and may form blood clots.

The pathogenesis during the infection process:

The pathogenesis of HEV infection in chickens is still unclear, but it is believed that avian HEVs, like mammalian HEVs, enter the host through the fecal oral route. The main replication sites of avian HEV in chickens are still unclear. It has been proven that when HEV is artificially infected in primates or pigs, the virus replicates in the liver. HEV replicates in liver cells and is released into the gallbladder, where it is then excreted from feces. In addition to the liver, replication type avian HEV can also be detected in the colon, cecum, and jejunum of artificially infected chickens at 5, 16, 20, and 35 days after infection, ileum at 7, 10, 20, and 35 days after infection, duodenum at 20 days after infection, and cecal tonsil brown at 35 and 56 days after infection. Therefore, oral inoculation of gastrointestinal tissue may be the first site of replication for avian HEV. However, the clinical and pathological significance of HEV replication in the extrahepatic region is still unclear.

immunityThe characteristic of humoral immune response in chickens infected with avian HEV is the production of IgG antibodies approximately 1-4 weeks after vaccination. The cellular immune response of chickens infected with avian HEV is still unclear. Like mammalian HEVs, the capsid protein of avian HEVs is an immunogenic protein that mediates a protective immune response against avian HEV infection. To demonstrate that the avian HEV capsid protein shares common antigenic determinants with porcine and human HEVs, and can generate cross immune responses. The avian HEV capsid protein can react with anti human (Sar-55 strain) serum and anti recovery serum of porcine HEV and HEV US 2 strains. On the contrary, the recovery serum of chickens artificially infected with avian HEV can also react with the recombinant capsid proteins of pigs and humans HEVs. Four antigenic domains (I, II, III, IV) have been identified in the avian HEV capsid protein. Guo et al. identified a B-cell epitope at the C-terminus of domain II (possibly at amino acid residues 477-492), which is unique to avian HEVs; Domain I (amino acid residues 389-410) has a B-cell epitope, which is possessed by avian, human, and porcine HEVs. All HEV strains identified so far belong to the same serotype.

diagnosisPreliminary diagnosis of HS syndrome can be made based on clinical symptoms and gross pathological changes or microscopic lesions. Hepatitis E HS syndrome must be distinguished from hemorrhagic fatty liver syndrome (HFLS) because HS syndrome presents with blood clots in the abdominal cavity, causing liver bleeding, and the liver in HS syndrome does not have fatty tissue like HFLS syndrome. When insecticides (anticoagulants) are poisoned, there may sometimes be blood clots (or none) in the abdominal cavity or around the liver. Differential diagnosis should also consider chicken trauma, liver bleeding, or perihepatic bleeding. Negative staining electron microscopy observation can pick up virus particles with a size of 30-50nm in the bile of chickens with HS syndrome.

At present, the diagnosis of HEV mainly uses RT-PCR to detect viral RNA and ELISA to detect viral antibodies. Merely using serological methods to detect acute avian HEV infection is not sufficient. In infected chickens, viremia and fecal detoxification occur earlier than the appearance of avian HEV IgG antibodies. Therefore, chickens with negative serological tests may still be infected with avian HEV. The avian HEV specific RT-PCR method has been successfully used for the detection of avian HEV infection in chicken flocks. A heterologous double strand shift method is used as a tool to identify avian HEV strains with genetic differences. At present, the identification of specific antigenic epitopes of avian HEV capsid proteins helps to further develop diagnostic methods for distinguishing infections caused by avian HEV, porcine HEV, or human HEV.

Preventive measures:

1. So far, there is no vaccine available for hepatitis E HEV. At present, there is no effective treatment for avian HEV infection. The use of drugs that protect the liver, kidneys, and enhance immune function can help with the recovery of this disease.

2. Strict implementation of biosecurity measures in chicken farms can limit the spread of viruses. Strictly select the source field of chicken seedlings to prevent vertical transmission.

3. Strengthen feeding management and use full price feed.

4. Controlling immunosuppressive diseases can reduce the infection of avian HEV.

In the past few years, I have seen several cases of liver rupture and blood clots on the liver in clinical practice. At first, it was thought to be fatty liver, but it was found to be different from common fatty liver. In addition to liver enlargement, bleeding, rupture, and blood clot coverage, this disease has very little abdominal fat deposition, and some are even very thin. The liver does not have the same fatty phenomenon as fatty liver, and treatment with choline chloride, vitamin E, methionine, etc. is ineffective. Zeng Baisi couldn't figure it out, but later verified avian pathology and found out that hepatitis E had similar changes to fatty liver. After multiple observations, it was suspected to be hepatitis E, but due to the lack of laboratory diagnostic methods and the failure to send it to relevant teaching and research units for testing, it could not be diagnosed. This year, during the clinical diagnosis training course on drug susceptibility testing, I heard from Professor Chang Weishan of Shannong University that hepatitis E is widely present in society, which helped me to relax and consider it as a problem with hepatitis E.