Histologic findings and viral antigen distribution in natural coinfection of layer hens with subgroup J avian leukosis virus, Marek’s disease virus, and reticuloendotheliosis virus

Li, Hongmei; Ma, Kui; Liu, Miaomiao; Yang, Chengcheng; Huang, Xueting; Zhao, Yu; Qi, Kezong

doi:10.1177/1040638719868274

Cited by 13 publications

(9 citation statements)

References 16 publications

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“…An increase occurs in size and irregularity of the Haversian canals, and there is an increase in the number, size and an alteration in the position of lacunae. These results partially agree with El-Gohary et al (2000) and Liu et al (2019) who described similar bone lesions in naturally infected chickens with ALV-J at the 27 th week old.…”

Section: Ne Ussupporting

confidence: 92%

“…This virus has (v-myc) gene which plays a role similar to those of (v-erbB) gene of erythroblastosis viruses in blocking erythroid precursor cell differentiation resulting in anemia (Pattison et al, 2008). Also, suppression of the hematopoiesis as a result of marked proliferation of tumor cells in the bone marrow was recorded by Liu et al (2019). The stained blood film of experimentally infected chicks revealed some erythrocytes abnormalities including anisocytosis, poikilocytosis, binucleated erythroblasts and increased number of polymorphic erythroblasts.…”

Section: Discussionmentioning

confidence: 99%

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Pathological, Clinicopathological and Molecular Investigations on Chickens Experimentally Infected with Avian Leucosis Virus Type J

Fotouh¹,

Soufy²,

M.B³

et al. 2020

Adv. Anim. Vet. Sci.

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Avian leucosis virus type J (ALV-J) causes highly economic losses in the production of meat and egg. This study aimed to investigate the effect of experimental infection of one-day-old chicks with ALV-J strain-local isolateon hemogram, biochemical constituents, ALV-J antibody titer, and histopathology of the internal organs. Detection of ALV-J DNA in the internal organs was also performed using the PCR technique. One hundred and twenty chicks-one day old-were randomly divided into two equal groups. The first group was infected intra-peritoneally with isolated ALV-J strain at a dose of 0.2 ml of log10 4 embryo infected dose (EID 50). The second group was kept as normal control and was inoculated intra-peritoneally with 0.2 ml of sterile saline. After inoculation, all experimental birds were kept under strict daily observation for recording clinical signs and mortality rates. At the 1 st , 2 nd , 3 rd , 4 th and 5 th month post-infection (mpi), blood and tissue samples were collected from each group for determination of hemogram, serum biochemical parameters, antibody titer, and histopathological and molecular examinations of the internal organs. The infected group showed dullness, ruffled feathers, droppings, loss of appetite, decrease in feed intake and depression. The mortality rate reached to18.3% in the infected group. Macrocytic normochromic anemia, leukocytosis, heterophilia, and lymphocytosis were recorded. Serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase activities, and creatinine and uric acid levels were markedly (P<0.05) increased. Lymphoid and myeloid leucosis in the heart, liver, spleen, and kidneys and also erythroid leucosis in the heart and osteopetrosis were recorded. In conclusion, the experimental infection with ALV-J caused alteration in the hemogram, dysfunction of liver and kidney as well as histopathological lesions in the internal organs and bone of infected chickens. These changes began at the 1 st mpi and can help in the early diagnosis of disease.

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Section: Ne Ussupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Pathological, Clinicopathological and Molecular Investigations on Chickens Experimentally Infected with Avian Leucosis Virus Type J

Fotouh¹,

Soufy²,

M.B³

et al. 2020

Adv. Anim. Vet. Sci.

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“…The supernatants were filtered through 0.22-μm filters and used for inoculation on the cell cultures. Another part was cut into a tissue cube 0.5 cm × 0.5 cm in size and fixed in 10% buffered formalin and then used for the histopathological observation according to routine procedures ( Liu et al., 2019 ).…”

Section: Methodsmentioning

confidence: 99%

An outbreak in three-yellow chickens with clinical tumors of high mortality caused by the coinfection of reticuloendotheliosis virus and Marek’s disease virus: a speculated reticuloendotheliosis virus contamination plays an important role in the case

Shi¹,

Li²,

Wang³

et al. 2021

Poultry Science

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Both reticuloendotheliosis and Marek's disease are neoplastic diseases of chickens caused by reticuloendotheliosis virus ( REV ) and Marek's disease virus ( MDV ), respectively. The infection of REV or MDV may lead to clinical tumors and also result in immunosuppression and easily allow secondary infection by other pathogens. Here, we investigated a breeder flock of three-yellow chickens in southern China that had been vaccinated with CVI988/Rispens at hatching and had experienced depression, weakness, reduction in weight gain, and an increased death rate after 120 d of age. The morbidity and mortality were 20% and 10%, respectively, at 140 d of age when this infection was diagnosed. The necropsy of the birds revealed significant tumor-like lesions in the heart, liver, spleen, and ceca. Peripheral blood lymphocytes and tumor-like tissues were sampled for PCR detection and for histopathological observation, for virus isolation and the subsequent immunofluorescent assay on the cell cultures and for gene sequencing of the isolated viruses. A REV isolate GX18NNR1 and a MDV isolate GX18NNM5 were both recovered from the sampled bird. Further phylogenetic analysis based on the env gene of REV and the meq gene of MDV demonstrated that GX18NNR1 was closely related to the reference REV strain MD-2, which was isolated from a contaminated commercial turkey herpesvirus vaccine. In addition, the GX18NNM5 was found to belong to the Chinese very virulent MDV strains' cluster. The coinfection of REV and MDV may contribute to tumor outbreaks with high morbidity and mortality in three-yellow chicken flocks.

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“…ALV-J and REV are transmitted both horizontally and vertically [ 5 , 6 ], and are the most common naturally occurring simple retroviruses associated with neoplastic and immunosuppressive diseases in poultry [ 7 , 8 , 9 , 10 ]. Owing to the similar characteristics and widespread nature of ALV-J and REV in the field, co-infection is common [ 11 , 12 , 13 , 14 , 15 , 16 ] and is an important emerging problem in chicken flocks. Synergism in ALV-J and REV co-infected chicken flocks causes higher mortality, more serious growth retardation, and immunosuppression [ 17 , 18 ], and facilitates viral replication and exosomal miRNA accumulation [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Musashi-1 and miR-147 Precursor Interaction Mediates Synergistic Oncogenicity Induced by Co-Infection of Two Avian Retroviruses

Zhou

Ding

et al. 2022

Cells

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Synergism between avian leukosis virus subgroup J (ALV-J) and reticuloendotheliosis virus (REV) has been reported frequently in co-infected chicken flocks. Although significant progress has been made in understanding the tumorigenesis mechanisms of ALV and REV, how these two simple oncogenic retroviruses induce synergistic oncogenicity remains unclear. In this study, we found that ALV-J and REV synergistically promoted mutual replication, suppressed cellular senescence, and activated epithelial-mesenchymal transition (EMT) in vitro. Mechanistically, structural proteins from ALV-J and REV synergistically activated the expression of Musashi-1(MSI1), which directly targeted pri-miR-147 through its RNA binding site. This inhibited the maturation of miR-147, which relieved the inhibition of NF-κB/KIAA1199/EGFR signaling, thereby suppressing cellular senescence and activating EMT. We revealed a synergistic oncogenicity mechanism induced by ALV-J and REV in vitro. The elucidation of the synergistic oncogenicity of these two simple retroviruses could help in understanding the mechanism of tumorigenesis in ALV-J and REV co-infection and help identify promising molecular targets and key obstacles for the joint control of ALV-J and REV and the development of clinical technologies.

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Histologic findings and viral antigen distribution in natural coinfection of layer hens with subgroup J avian leukosis virus, Marek’s disease virus, and reticuloendotheliosis virus

Cited by 13 publications

References 16 publications

Pathological, Clinicopathological and Molecular Investigations on Chickens Experimentally Infected with Avian Leucosis Virus Type J

Pathological, Clinicopathological and Molecular Investigations on Chickens Experimentally Infected with Avian Leucosis Virus Type J

An outbreak in three-yellow chickens with clinical tumors of high mortality caused by the coinfection of reticuloendotheliosis virus and Marek’s disease virus: a speculated reticuloendotheliosis virus contamination plays an important role in the case

Musashi-1 and miR-147 Precursor Interaction Mediates Synergistic Oncogenicity Induced by Co-Infection of Two Avian Retroviruses

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