Co-infection with avian hepatitis E virus and avian leukosis virus subgroup J as the cause of an outbreak of hepatitis and liver hemorrhagic syndromes in a brown layer chicken flock in China

Sun, Yani; Lu, Qizhong; Zhang, Jingfei; Li, Xiaoxuan; Zhao, Jian; Fan, Wenqi; Ji, Pinpin; Wang, Kun; Zhou, En‐Min; Zhao, Qin

doi:10.1016/j.psj.2019.10.067

Cited by 16 publications

(12 citation statements)

References 36 publications

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“…In general, the immunotolerance state is a prerequisite for tumorigenesis. During congenital infection of ALV-J, the cellular and humoral immune systems are severely damaged [ 7 , 8 ], increasing the probability of chicken secondary infection by bacteria or viruses and mortality to a degree of magnitude higher than that caused by simple tumors induced by non-immunosuppressive viruses [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

High-frequency and activation of CD4+CD25+ T cells maintain persistent immunotolerance induced by congenital ALV-J infection

Zheng

Zhou

et al. 2021

Vet Res

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Congenital avian leukosis virus subgroup J (ALV-J) infection can induce persistent immunotolerance in chicken, however, the underlying mechanism remains unclear. Here, we demonstrate that congenital ALV-J infection induces the production of high-frequency and activated CD4+CD25+ Tregs that maintain persistent immunotolerance. A model of congenital infection by ALV-J was established in fertilized eggs, and hatched chicks showed persistent immunotolerance characterized by persistent viremia, immune organ dysplasia, severe imbalance of the ratio of CD4+/CD8+ T cells in blood and immune organs, and significant decrease in CD3+ T cells and Bu-1+ B cells in the spleen. Concurrently, the mRNA levels of IL-2, IL-10, and IFN-γ showed significant fluctuations in immune organs. Moreover, the frequency of CD4+CD25+ Tregs in blood and immune organs significantly increased, and the frequency of CD4+CD25+ Tregs was positively correlated with changes in ALV-J load in immune organs. Interestingly, CD4+CD25+ Tregs increased in the marginal zone of splenic nodules in ALV-J-infected chickens and dispersed to the germinal center. In addition, the proliferation and activation of B cells in splenic nodules was inhibited, and the number of IgM+ and IgG+ cells in the marginal zone significantly decreased. We further found that the mRNA levels of TGF- β and CTLA-4 in CD4+CD25+ Tregs of ALV-J-infected chickens significantly increased. Together, high-frequency and activated CD4+CD25+ Tregs inhibited B cells functions by expressing the inhibitory cytokine TGF-β and inhibitory surface receptor CTLA-4, thereby maintaining persistent immunotolerance in congenital ALV-J-infected chickens.

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Section: Introductionmentioning

confidence: 99%

High-frequency and activation of CD4+CD25+ T cells maintain persistent immunotolerance induced by congenital ALV-J infection

Zheng

Zhou

et al. 2021

Vet Res

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“…Therefore, there is few reports of ALV-J infection in layers in recent years. Zhao discovered that co-infection with avian hepatitis E virus and avian leukosis virus subgroup J is the cause of an outbreak of hepatitis and liver hemorrhagic syndromes in a Hy-line brown layer chicken ock in China recently [19]. This study also found subclinical infection of ALV-J in the roosters of Hy-line layers, which reminded us that the puri cation of ALV can not be overlooked, and needs to be continued through monitoring by proportional sampling.…”

Section: Discussionmentioning

confidence: 65%

Re-emergence of Avian leukosis virus subgroup J in the rooster of Hy-line brown layers and its transmission pattern in flocks

Meng

Gao³

et al. 2021

Preprint

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Avian leukosis virus subgroup J (ALV-J) is the most prevalent subgroup in chickens and exhibits increasing pathogenicity and stronger horizontal and vertical transmission ability among different kinds of chickens. Although vertical transmission of ALV-J from hens infected through artificial insemination was reported before by the detection of swabs and serum, but there was no further research on the transmission pattern of ALVs in the roosters. In the present study, the introduction of Hy-line brown roosters significantly increased the p27 positive rate of ALV in an indigenous flock detected by ELISA and virus isolation. Sequence analysis and IFA showed that it is classified into ALV-J subgroup, locating in a new branch compared with the domestic and foreign referential sequences. Meanwhile, the gp85 gene of the ALV-J isolated in the hens and its albumens had a homology of 94.1–99.7% with that in the roosters, which means that the strain is quite likely transmitted to the hens and their offspring through insemination of the roosters. In addition, there are four ALV-J infection status in plasma and semen of rooster (V + S+, V-S+, V + S-, V-S-), so the eradication of ALV in rooster requires simultaneous virus isolation of semen and plasma. Additionally, compared with ALV detection in samples by DF-1 cells, directly detecting ALV in semen by ELISA exists some false positives. Collectively, our results suggested that the incomplete eradication process of roosters leads to the sporadic findings of ALV-J in laying hens

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“…Actually, it has been reported mixed infections of avian HEV and ALV [4], HEV and MDV since 2016 [14], and the mixed infection rate of avian HEV and several immunosuppressive viruses was up to 58% in chickens, China, including CIAV, ALV, and REV [5], which indicated that the mixed infections of HEV and other viruses were common in chicken ocks. In the current study, further PCR detection showed that all 11 HEV positive samples were mixed infections, of which the infection rates of HEV and CIAV, HEV and FAdV were highest.…”

Section: Discussionmentioning

confidence: 99%

“…Avian HEV is a member of hepevirus and possesses a single-stranded positive-sense RNA genome of approximately 6.6 kb in size, which contains three open reading frames (ORFs) and 3' and 5' non-coding regions. Of which, capsid protein encoded by ORF2 is highly conserved and has been extensively used for viral genotyping and genetic evolution analysis of HEV [4].…”

Section: Introductionmentioning

confidence: 99%

“…Recently, the outbreak of hepatosplenomegaly disease has been increased in chickens, although avian HEV is considered to be the major causative agent, fowl adenovirus (FAdV), reticuloendotheliosis virus (REV), avian leukosis virus (ALV), Marek's disease virus (MDV) and chicken infectious anaemia virus (CIAV) can also cause hepatosplenomegaly and immunosuppression, which may facilitate the popularity of avian HEV [4,5], hence, the continual epidemiological investigation of avian HEV is necessary. In the present study, the suspected cases of avian HEV infection were diagnosed, and the molecular epidemiology of avian HEV in chickens was characterized in Shandong Province between 2020 and 2021.…”

Section: Introductionmentioning

confidence: 99%

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The Diagnosis and Molecular Epidemiology Investigation of Avian Hepatitis E in Shandong Province, China

Liu

Zhao

et al. 2021

Preprint

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Background: Avian hepatitis E virus (HEV) is the pathogenic agent of big liver and spleen disease (BLS) and hepatitis-splenomegaly syndrome (HS) in chickens, which has caused economic losses to the poultry industry in China. Eighteen samples of BLS chickens were collected in this study to understand the molecular epidemiology characteristics of avian HEV in Shandong province, China.Results: Gross and microscopic lesions of clinical samples were observed, then virology detection and genetic analysis of avian HEV were performed. The results showed that there were significant swelling and rupture in the liver, and spleen was enlarged. Microscopic lesions demonstrated that obvious hemorrhage in the liver, with infiltration of heterophilic granulocytes, lymphocytes, and macrophages, the reduction of lymphocytes in the spleen. Eleven out of the 18 samples were positive for HEV, with a positive rate of 61.11%. More importantly, all HEV positive samples were mixed infections. Among them, the mixed infections of avian HEV and chicken infectious anaemia virus (CIAV) and fowl adenovirus (FAdV) were the most common. In addition, the genetic evolution analysis showed that all obtained HEV isolates did not belong to the reported 4 genotypes, and they constituted a novel genotype. Conclusions: These results of this study further enriched the epidemiological data of avian HEV in Shandong province and proved the genetic diversity of HEV in China, but also uncovered the complicated mixed infections of avian HEV in clinical.

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Co-infection with avian hepatitis E virus and avian leukosis virus subgroup J as the cause of an outbreak of hepatitis and liver hemorrhagic syndromes in a brown layer chicken flock in China

Cited by 16 publications

References 36 publications

High-frequency and activation of CD4+CD25+ T cells maintain persistent immunotolerance induced by congenital ALV-J infection

High-frequency and activation of CD4+CD25+ T cells maintain persistent immunotolerance induced by congenital ALV-J infection

Re-emergence of Avian leukosis virus subgroup J in the rooster of Hy-line brown layers and its transmission pattern in flocks

The Diagnosis and Molecular Epidemiology Investigation of Avian Hepatitis E in Shandong Province, China

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