Growth of Duck Hepatitis Virus in Chicken Embryos and in Cell Cultures Derived from Infected Embryos

Mason, Richard; Tauraso, Nicola M.; Ginn, Robert K.

doi:10.2307/1588819

Cited by 8 publications

(5 citation statements)

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“…The DHAV‐1 H strain (GenBank: JQ301467.1) was used throughout the present study. The virus was propagated in 10‐day‐old duck embryos according to standard procedures and harvested from the allantoic fluids of deceased embryos at 36–72 hr post‐infection (Mason et al., 1972; Stoute et al., 2020). The collected virus was stored at −80°C.…”

Section: Methodsmentioning

confidence: 99%

Duck hepatitis A virus 1 has lymphoid tissue tropism altering the organic immune responses of mature ducks

Mao

Wang

et al. 2021

Transbound Emerg Dis

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Duck hepatitis A virus 1 (DHAV‐1) is a highly prevalent pathogen within adult ducks causing acute as well as chronic hepatitis which closely emulates the progression of human hepatitis. However, the underlying mechanisms of DHAV‐1 persistence and the pathogenesis of chronic liver disease are not well defined. The association between hematopoietic reservoirs of virus and persistent infection is increasingly concerning. Here, we explored the ability of lymphoid replication of DHAV‐1 and the effect on immunity. We found that DHAV‐1 was able to infect and replicate productively in the lymphoid organs of model ducks, persisting over 6 months. Moreover, a significant correlation of viral loads between these organs and blood was found, documenting a major contribution of lymphoid replication to DHAV‐1 viraemia. Along with viral replication, the mRNA of PRRs and immune‐related cytokines was up‐regulated in these organs during the early phase of infection, showing tissue‐dependent expression patterns but all inclining towards Th2 responses due to the consistently higher level of IL‐4 than IL‐2 and IFN‐γ. Additionally, the expression of CCL19, CCL21, MHC‐I and MHC‐II, which are involved in T cell homing to the periphery and priming, was dysmodulated. Our data indicate that DHAV‐1 possesses lymphoid tissue tropism, contributing to persistent infection and chronic hepatitis via altering the early endogenous transcription of immune‐related genes and thereby perturbing organic immunity. These results may be useful to develop novel strategies to treat chronic viral hepatitis based on stimulation of the early innate system and regulation of T‐cell trafficking.

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Section: Methodsmentioning

confidence: 99%

Duck hepatitis A virus 1 has lymphoid tissue tropism altering the organic immune responses of mature ducks

Mao

Wang

et al. 2021

Transbound Emerg Dis

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“…The DHAV-1 H strain (GenBank: JQ301467.1) was selected to investigate its replication and effects on the immune responses of adult ducks. The virus was propagated in 10-day-old duck embryos by standard procedures and harvested from allantoic fluids of deceased duck embryos at 36–72 h post-infection ( 4 , 22 ). Virus at a concentration of 4.56 × 10 8 copies/mL determined by quantitative real-time PCR (qPCR) was used to infect ducks ( 23 ).…”

Section: Methodsmentioning

confidence: 99%

Virologic and Immunologic Characteristics in Mature Ducks with Acute Duck Hepatitis A Virus 1 Infection

Mao

Wang

et al. 2017

Front. Immunol.

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Duck hepatitis A virus 1 (DHAV-1) infection in mature ducks has previously been proposed as a small-animal model for human hepatitis A. However, basic research on the outcome of DHAV-1 infection in mature ducks is limited. Here, we examined the course of viremia, the characteristics of antibody responses, and the profiles of plasma cytokines in mature ducks infected with DHAV-1. During the course of infection, the viremia was detectable soon after infection and persisted for 196 days, however, the ducks presented as clinically asymptomatic. Specific and timely immunoglobulin G (IgG), IgM, and IgA1 responses were elicited. At the same time, extensive inhibition of viral replication was observed with increasing IgG concentration. With respect to pattern-recognition receptors, TLR-7 was mainly involved in triggering the innate defense against the DHAV-1 infection. In addition, plasma immune analytes were measured and were determined to have bidirectional roles in virus clearance. It was concluded that DHAV-1 spreads quickly in blood. The spontaneous clearance of DHAV-1 during asymptomatic infection in mature ducks depends on the cooperation of timely antibody responses and alert innate immune responses. Moreover, the delayed clearance may be associated with a weak interferon-γ-producing CD8+ T cell response. This study allows us to reveal the mechanism of clearance and persistence of DHAV-1 infection in mature ducks. We anticipate that it will provide a basis for future studies focused on defining the nature mechanisms involved in the clearance and persistence of human hepatitis virus.

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“…Hepadnaviruses are known to produce acute-to-chronic hepatitis and/or hepatocellular carcinoma in human, woodchucks, ground squirrels, and pekin ducks (3,6,11,13,15,22,30,31,32,37). Experimental transmission of pekin duck hepatitis B virus to domestic geese has been recently reported (20). In this recent study, unsuccessful transmission of virus to domestic chicks was reported, but domestic turkeys were not included in the study.…”

Section: Turkey Viral Hepatitis (Tvh) Was First Described In 1959 By mentioning

confidence: 99%

Experimental Transmission of Turkey Viral Hepatitis to Day-Old Poults and Identification of Associated Viral Particles Resembling Picornaviruses

Klein¹,

Castro²,

Meteyer³

et al. 1991

Avian Diseases

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Turkey viral hepatitis (TVH) was experimentally reproduced in two experiments in 1-day-old poults. In the first experiment, an infectious inoculum was prepared from filtered yolk materials harvested from dead embryonating chicken eggs (ECE) previously inoculated with suspensions of liver and pancreas tissues collected from TVH-affected birds in commercial turkey flocks. One-day-old poults given a yolk-sac inoculation or oral gavage with this preparation developed lesions in the liver and pancreas characteristic of TVH at 20 days postinoculation (PI) in 60% and 14% of the experimentally infected birds, respectively. With the identical inoculum, embryo mortality occurred at 8 and 10 days PI in embryonating turkey eggs (ETE) inoculated into the yolk sac. In the second experiment, an infectious inoculum was prepared from filtered yolk materials from dead ETE harvested in the first experiment. One-day-old poults given a yolk-sac inoculation with this filtered yolk material developed lesions in the liver and pancreas within 5 days PI. At 20 days PI, 67% of the experimentally infected birds had similar lesions. With the inoculum given to these poults, embryo mortality occurred at 6, 8, and 10 days PI in ETE inoculated into the yolk sac. Virus particles 26-28 nm in diameter with icosahedral morphology typical of picornaviruses were identified by EM in the yolk sacs of ETE that died in both experiments, and inoculated ETE that died following passage of filtered suspensions of pancreatic tissues collected from affected birds in the first experiment.

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Growth of Duck Hepatitis Virus in Chicken Embryos and in Cell Cultures Derived from Infected Embryos

Cited by 8 publications

References 0 publications

Duck hepatitis A virus 1 has lymphoid tissue tropism altering the organic immune responses of mature ducks

Duck hepatitis A virus 1 has lymphoid tissue tropism altering the organic immune responses of mature ducks

Virologic and Immunologic Characteristics in Mature Ducks with Acute Duck Hepatitis A Virus 1 Infection

Experimental Transmission of Turkey Viral Hepatitis to Day-Old Poults and Identification of Associated Viral Particles Resembling Picornaviruses

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