Duck viral hepatitis is an acute, highly contagious, viral disease of young ducklings characterized by a short incubation period, sudden onset, high mortality, and characteristic liver lesions. The disease is of economic importance in all duck-raising areas of the world. Three distinct types of duck hepatitis virus (DHV) have been isolated from diseased ducklings.The originally described, most widespread, and most virulent DHV Type I is an enterovirus in the family Picornaviridae and is readily propagated in chick and duck embryos. It does not produce hemagglutinins. Field experience with DHV Type I indicates that egg transmission does not occur. The disease can be transmitted experimentally by parenteral or oral administration of infected tissues. Viruses differing from classic DHV Type I have been recognized as causes of hepatitis in ducklings. DHV Type II is considered to be an astrovirus and is difficult to propagate under laboratory conditions; DHV Type III is a member of the Picornaviridae, is antigenically distinct from Type I virus, and can be propagated in duck (but not chick) embryos. A distinct serologic variant of DHV Type I, named DHV Type Ia, has also been described (Merck Vet Manual: Duck Viral Hepatitis).
4. Host Ranges and Animal Models
A natural outbreak of DHV Type I has been reported in mallard ducklings; experimental DHV Type I infections have been produced in goslings, turkey poults, young pheasants, quail, and guinea fowl. The viruses that cause hepatitis in ducklings should not be confused with duck hepatitis B virus, a hepadnavirus infection of older ducks (Merck Vet Manual: Duck Viral Hepatitis).
Immune Response:
DHV-1-specific antibodies, neutralizing antibodies and lymphocyte proliferation were well induced in ducklings (Fu et al., 2012).
Efficacy:
Vaccination with pSCA/VP1 could significantly reduce the onset and duration of viremia and decrease virus replication in ducklings (Fu et al., 2012).
(Yang et al., 2021)The P1-P2A-3C cassette was inserted into the gene junction between UL26 and UL27 in the DEV vaccine strain genome. For transfection, we used the modified fosmids, C144-UL26/27-P13C, which replaced the parental fosmid C144. After being blindly passaged once in CEFs, DEV-typical plaques appeared in the CEFs transfected with the DNA combinations. Electron microscopy confirmed the successful rescue of the recombinant viruses. Insertion of the P1-P2A-3C cassette at the proper site was confirmed by PCR and sequencing, using a forward primer specific to the P1 gene and a reverse primer matching the UL26 sequence. The recombinant DEV was designated rDEV-UL26/27-P13C, with the P1 and 3C genes inserted between UL26 and UL27, in the DEV genome.
h. Immunization Route
Intramuscular injection (i.m.)
i.
Ducks Response
Vaccination Protocol:
(Yang et al., 2021) Groups of 20 ducks were inoculated with 1000 ELD50 of the recombinant viruses to evaluate the antibody responses against DHAV-3 and DEV induced by the recombinant DEVs.
Challenge Protocol:
(Yang et al., 2021) All the animal experiments were performed using SPF ducks housed in filtered-air, negative-pressure isolation units. The ducks were given free access to food and water. To evaluate the protective efficacy of the recombinant viruses against challenge by the virulent DHAV-3 and DEV, each group of 20 ducks was inoculated subcutaneously with 1,000 times the 50% egg lethal dose (1000 ELD50) of the rescued viruses at 1 day of age. At 7 days post-vaccination, 10 ducks in each group were intramuscularly challenged with 100 ELD50 of the virulent DHAV-3 A3 strain, and the remaining 10 ducks were intramuscularly challenged with 1,000 minimum lethal doses of the virulent DEV CSC strain. Ten unvaccinated and unchallenged ducks were used as the healthy controls. The ducks were examined for clinical signs and mortality for 2 weeks after the challenge. The dead and surviving ducks were observed for gross lesions in the liver, spleen, kidneys, esophagus, intestine, thymus, and bursa.
Description:
(Yang et al., 2021) The ducks were inoculated with the recombinant viruses at 1 day of age and challenged with the virulent DHAV-3 A3 strain 7 days post-inoculation for protective efficacy evaluation. These ducks did not show any clinical signs in response to vaccination before the challenge. The ducks in the rDEV-UL26/27-P13C vaccination group were completely protected from lethal DHAV-3 challenge, showing no clinical signs of disease and no visible lesions in the liver, spleen, or other organs during the 2-week observation period. However, all ducks in the challenge control group showed severe clinical signs from 2 days post-challenge, including depression, lethargy, and anorexia; all these ducks died from the DHAV-3 challenge within 3 days. As expected, the ducks in the healthy control group did not show any clinical signs during the experiment. These results indicate that rDEV-UL26/27-P13C induced 100% protection against lethal DHAV-3 challenge in ducks.
(Yang et al., 2021) The P1-P2A-3C cassette was inserted into the gene junction between US7 and US8 in the DEV vaccine strain genome. For transfection, we used the modified fosmid C343-US7/8-P13C, which replaced the parental fosmid C343. After being blindly passaged once in CEFs, DEV-typical plaques appeared in the CEFs transfected with the DNA combinations. Electron microscopy confirmed the successful rescue of the recombinant viruses. Insertion of the P1-P2A-3C cassette at the proper site was confirmed by PCR and sequencing, using a forward primer specific to the P1 gene and a reverse primer matching the US8 sequence. The recombinant DEVs was designated rDEV-US7/8-P13C, with the P1 and 3C genes inserted between US7 and US8, in the DEV genome.
h. Immunization Route
Intramuscular injection (i.m.)
i. Description
A bivalent duck hepatitis virus recombinant vector vaccine that is made of a P1-P2a-33 cassette inserted between US7 and US8 of the viral genome (Yang et al., 2021).
j.
Ducks Response
Vaccination Protocol:
(Yang et al., 2021) Groups of 20 ducks were inoculated with 1000 ELD50 of the recombinant viruses to evaluate the antibody responses against DHAV-3 and DEV induced by the recombinant DEVs.
Challenge Protocol:
(Yang et al., 2021)All the animal experiments were performed using SPF ducks housed in filtered-air, negative-pressure isolation units. The ducks were given free access to food and water. To evaluate the protective efficacy of the recombinant viruses against challenge by the virulent DHAV-3 and DEV, each group of 20 ducks was inoculated subcutaneously with 1,000 times the 50% egg lethal dose (1000 ELD50) of the rescued viruses at 1 day of age. At 7 days post-vaccination, 10 ducks in each group were intramuscularly challenged with 100 ELD50 of the virulent DHAV-3 A3 strain, and the remaining 10 ducks were intramuscularly challenged with 1,000 minimum lethal doses of the virulent DEV CSC strain. Ten unvaccinated and unchallenged ducks were used as the healthy controls. The ducks were examined for clinical signs and mortality for 2 weeks after the challenge. The dead and surviving ducks were observed for gross lesions in the liver, spleen, kidneys, esophagus, intestine, thymus, and bursa.
Description:
(Yang et al., 2021) The ducks were inoculated with the recombinant viruses at 1 day of age and challenged with the virulent DHAV-3 A3 strain 7 days post-inoculation for protective efficacy evaluation. These ducks did not show any clinical signs in response to vaccination before the challenge. The ducks in the rDEV-US7/8-P13C vaccination group were completely protected from lethal DHAV-3 challenge, showing no clinical signs of disease and no visible lesions in the liver, spleen, or other organs during the 2-week observation period. However, all ducks in the challenge control group showed severe clinical signs from 2 days post-challenge, including depression, lethargy, and anorexia; all these ducks died from the DHAV-3 challenge within 3 days. As expected, the ducks in the healthy control group did not show any clinical signs during the experiment. These results indicate that rDEV-US7/8-P13C induced 100% protection against lethal DHAV-3 challenge in ducks.
4. Duck Virus Hepatitis Modified Live Virus Vaccine (USDA: 14B1.10)
1. Fu et al., 2012: Fu Y, Chen Z, Li C, Liu G. Protective immune responses in ducklings induced by a suicidal DNA vaccine of the VP1 gene of duck hepatitis virus type 1. Veterinary microbiology. 2012; 160(3-4); 314-318. [PubMed: 22819169].
