scholarly journals Morphological and Immunohistochemical Examination of Lymphoproliferative Lesions Caused by Marek’s Disease Virus in Breeder Chickens

Animals ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 1280
Author(s):  
Alessandro Stamilla ◽  
Antonino Messina ◽  
Lucia Condorelli ◽  
Francesca Licitra ◽  
Francesco Antoci ◽  
...  
Keyword(s):  
Mortality Rate ◽  
Marek's Disease ◽  
Neoplastic Disease ◽  
Marek’S Disease ◽  
Immunohistochemical Examination ◽  
Chicken Flock ◽  
Vaccination Programs ◽  
Microscopic Evaluation ◽  
Cecal Tonsil ◽  
Overall Mortality

Marek’s disease is widely controlled by vaccination programs; however, chickens are not totally protected, especially immediately after the vaccination when a strong challenge could interfere with the effectiveness of vaccination in the absence of proper biosecurity practice. This case report describes the occurrence of Marek’s disease (MD) observed in a breeder chicken flock reared southeast of Sicily. MD outbreak occurred from 32 to 47 weeks with an increase in weekly mortality rate (+0.4–0.6%). Overall, mortality rate related to Marek’s disease was about 6% at the end of the cycle. Carcasses of chickens found during the occurrence of disease underwent necropsy, and tissues were collected to confirm the infection. Gizzard, cecal tonsil, intestine, spleen and tumor mass were collected and analyzed from a carcass of one hen, 32 weeks old and apparently asymptomatic. Multiplex real-time PCR performed on spleen tissues detected the presence of MD virus pathogenic strain. Macroscopic and microscopic evaluation of the rest of the samples confirmed the neoplastic disease. Moreover, the immunophenotype of the tumor cells was identified as CD3 positive by immunohistochemical (IHC) staining. The vaccinated flock had become rapidly infected with the MD virus, which proves that the challenge of the MD virus was too strong in the rearing house at the beginning of the cycle, causing the outbreak.

scholarly journals Genome-wide characterization of copy number variations in the host genome in genetic resistance to Marek's disease using next generation sequencing

2020 ◽  
Author(s):  
Hao Bai ◽  
Yanghua He ◽  
Yi Ding ◽  
Huanmin Zhang ◽  
Jilan Chen ◽  
...  
Keyword(s):  
Next Generation Sequencing ◽  
Copy Number ◽  
Marek's Disease ◽  
Neoplastic Disease ◽  
Marek’S Disease ◽  
Next Generation ◽  
Qrt Pcr ◽  
Genome Wide ◽  
A Genome ◽  
Generation Sequencing

Abstract Background: Marek’s disease (MD) is a highly neoplastic disease primarily affecting chickens, and remains as a chronic infectious disease that threatens the poultry industry. Copy number variation (CNV) has been examined in many species and is recognized as a major source of genetic variation that directly contributes to phenotypic variation such as resistance to infectious diseases. Two highly inbred chicken lines 63 (MD-resistant) and 72 (MD-susceptible), as well as their F1 generation and six recombinant congenic strains (RCSs) with varied susceptibility to MD, are considered as ideal models to identify the complex mechanisms of genetic and molecular resistance to MD.Results: In the present study, to unravel the potential genetic mechanisms underlying resistance to MD, we performed a genome-wide CNV detection using next generation sequencing on the inbred chicken lines with the assistance of CNVnator. As a result, a total of 1,649 CNV regions (CNVRs) were successfully identified after merging all the nine datasets, of which 90 CNVRs were overlapped across all the chicken lines. Within these shared regions, 1,360 harbored genes were identified. In addition, 55 and 44 CNVRs with 62 and 57 harbored genes were specifically identified in line 63 and 72, respectively. Bioinformatics analysis showed that the nearby genes were significantly enriched in 36 GO terms and 6 KEGG pathways including JAK/STAT signaling pathway. Ten CNVRs (nine deletions and one duplication) involved in 10 disease-related genes were selected for validation by using qRT-PCR, all of which were successfully confirmed. Finally, qRT-PCR was also used to validate two deletion events in line 72 that were definitely normal in line 63. One high-confidence gene, IRF2 was identified as the most promising candidate gene underlying resistance and susceptibility to MD in view of its function and overlaps with data from previous study.Conclusions: Our findings provide valuable insights for understanding the genetic mechanism of resistance to MD and the identified gene and pathway could be considered as the subject of further functional characterization.

scholarly journals Detection of p53 mutation and serum monitoring alert caused by Marek's disease virus

2020 ◽  
Author(s):  
Huixia Zhang ◽  
Mengda Liu ◽  
Hui Zhang ◽  
Shengliang Cao ◽  
Yue Li ◽  
...  
Keyword(s):  
Point Mutation ◽  
Suppressor Gene ◽  
P53 Mutation ◽  
Marek's Disease ◽  
Economic Losses ◽  
Neoplastic Disease ◽  
Marek’S Disease ◽  
Infected Chicken ◽  
Serum Monitoring ◽  
Risk Of Cancer

Abstract Background Marek’s disease (MD), as a chicken neoplastic disease, brings huge economic losses to the global poultry industry. The tumor suppressor gene, wild type P53 plays a key role in blocking cell cycle, promoting apoptosis and maintaining stability of genome. The p53 function could change to that of an oncogene from a tumor inhibitory role, if a mutation happened. It will increase risk of cancer incidence. Results It was found that the mutation rate of p53 was 60 percent in experimentally infected and naturally infected chickens. The mutations included point-mutation and deletions, and mostly located in the DNA-binding domain. The most common point mutation happened in five sites, which were 651, 786, 828, 864 and 879 respectively. The mutated P53 can be expressed in tumors of various tissues in an infected chicken because of the lengthening of the half-life of mutated P53. Due to the loss of nuclear localization function, most of mutated P53 were expressed in cytoplasm. The concentration of P53 was decrease in serum of MD infected chicken. Conclusions Results of the current study suggested that p53 mutations with different types were common in MD, and most of mutated P53 were expressed in cytoplasm. Detecting the concertation of P53 and P53 antibody in serum could be helpful for diagnosis and monitor of MD.

scholarly journals Detection of p53 mutation and serum monitoring alert caused by Marek’s disease virus in poultry

2020 ◽  
Vol 16 (1) ◽  
Author(s):  
Huixia Zhang ◽  
Mengda Liu ◽  
Hui Zhang ◽  
Shengliang Cao ◽  
Yue Li ◽  
...  
Keyword(s):  
Human Cancer ◽  
Point Mutations ◽  
Suppressor Gene ◽  
Marek's Disease ◽  
Economic Losses ◽  
Control Group ◽  
Neoplastic Disease ◽  
Mutant P53 ◽  
Marek’S Disease ◽  
Infected Chicken

Abstract Background Marek’s disease (MD) is a chicken neoplastic disease, which brings huge economic losses to the global poultry industry. The wild type p53, a tumor suppressor gene, plays a key role in blocking cell cycle, promoting apoptosis, and maintaining the stability of the genome. However, the mutant p53 losses its tumor inhibitory role and become an oncogene when a mutation has happened. Results The mutation rate of p53 was 60% in the experimentally and naturally infected chickens. The mutations included point-mutations and deletions, and mostly located in the DNA-binding domain. The mutated p53 was expressed in various tumor tissues in an infected chicken. The mutant P53 proteins were notably accumulated in the cytoplasm due to the loss in the function of nuclear localization. Unlike the study on human cancer, the concentrations of P53 in the serums of MD infected chicken were significantly lower than the control group. Conclusions The p53 mutations were apparent in the development of MD. P53 and P53 antibody level in serum could be a useful marker in the diagnosis and surveillance of MD.

scholarly journals MicroRNAs 221 and 222 target p27Kip1 in Marek's disease virus-transformed tumour cell line MSB-1

2009 ◽  
Vol 90 (5) ◽  
pp. 1164-1171 ◽  
Author(s):  
Luke S. Lambeth ◽  
Yongxiu Yao ◽  
Lorraine P. Smith ◽  
Yuguang Zhao ◽  
Venugopal Nair
Keyword(s):  
Cell Cycle ◽  
Cell Line ◽  
Disease Virus ◽  
Expression Profiles ◽  
Marek's Disease Virus ◽  
Marek's Disease ◽  
Tumour Cell Line ◽  
Neoplastic Disease ◽  
Marek’S Disease Virus ◽  
Marek’S Disease

MicroRNAs (miRNAs) are a class of short RNAs that function as post-transcriptional suppressors of protein expression and are involved in a variety of biological processes, including oncogenesis. Several recent studies have implicated the involvement of miR-221 and miR-222 in tumorigenesis as these miRNAs are upregulated in a number of cancers and affect the expression of cell cycle regulatory proteins such as the cyclin-dependent kinase (cdk) inhibitor p27Kip1. Marek's disease virus (MDV) is a highly oncogenic herpesvirus that affects poultry, causing acute neoplastic disease with lymphomatous lesions in several organs. MDV-encoded oncogenes such as Meq are directly implicated in the neoplastic transformation of T cells and have been well studied. More recently, however, the involvement of both host and virus-encoded miRNAs in the induction of MD lymphomas is being increasingly recognized. We analysed the miRNA expression profiles in the MDV-transformed lymphoblastoid cell line MSB-1 and found that endogenous miRNAs miR-221 and miR-222 were significantly upregulated. Demonstration of the conserved binding sites for these miRNAs in the chicken p27Kip1 3′-untranslated region sequence and the repression of luciferase activity of reporter constructs indicated that miR-221 and miR-222 target p27Kip1 in these cells. We also found that overexpression of miR-221 and miR-222 decreased p27Kip1 levels and that treatment with retrovirally expressed antagomiRs partially alleviated this suppression. These data show that an oncogenic herpesvirus, as in the case of many cancers, can exploit the miRNA machinery for suppressing cell cycle regulatory molecules such as p27Kip1 in the induction and progression of T-cell lymphomas.

scholarly journals MicroRNA Profile of Marek's Disease Virus-Transformed T-Cell Line MSB-1: Predominance of Virus-Encoded MicroRNAs

2008 ◽  
Vol 82 (8) ◽  
pp. 4007-4015 ◽  
Author(s):  
Yongxiu Yao ◽  
Yuguang Zhao ◽  
Hongtao Xu ◽  
Lorraine P. Smith ◽  
Charles H. Lawrie ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Line ◽  
Disease Virus ◽  
Northern Blotting ◽  
Marek's Disease Virus ◽  
Marek's Disease ◽  
Neoplastic Disease ◽  
Marek’S Disease Virus ◽  
Marek’S Disease ◽  
Microrna Profile

ABSTRACT Research over the last few years has demonstrated the increasing role of microRNAs (miRNAs) as major regulators of gene expression in diverse cellular processes and diseases. Several viruses, particularly herpesviruses, also use the miRNA pathway of gene regulation by encoding their own miRNAs. Marek's disease (MD) is a widespread lymphomatous neoplastic disease of poultry caused by the highly contagious Marek's disease virus type 1 (MDV-1). Recent studies using virus-infected chicken embryo fibroblasts have identified at least eight miRNAs that map to the RL/RS region of the MDV genome. Since MDV is a lymphotropic virus that induces T-cell lymphomas, analysis of the miRNA profile in T-cell lymphoma would be more relevant for examining their role in oncogenesis. We determined the viral and host miRNAs expressed in MSB-1, a lymphoblastoid cell line established from an MDV-induced lymphoma of the spleen. In this paper, we report the identification of 13 MDV-1-encoded miRNAs (12 by direct cloning and 1 by Northern blotting) from MSB-1 cells. These miRNAs, five of which are novel MDV-1 miRNAs, map to the Meq and latency-associated transcript regions of the MDV genome. Furthermore, we show that miRNAs encoded by MDV-1 and the coinfected MDV-2 accounted for >60% of the 5,099 sequences of the MSB-1 “miRNAome.” Several chicken miRNAs, some of which are known to be associated with cancer, were also cloned from MSB-1 cells. High levels of expression of MDV-1-encoded miRNAs and potentially oncogenic host miRNAs suggest that miRNAs may have major roles in MDV pathogenesis and neoplastic transformation.

Marek's Disease Virus-Induced Transient Cecal Tonsil Atrophy

2014 ◽  
Vol 58 (2) ◽  
pp. 262-270 ◽  
Author(s):  
Mohammad Heidari ◽  
Scott D. Fitzgerald ◽  
Huanmin Zhang
Keyword(s):  
Disease Virus ◽  
Marek's Disease Virus ◽  
Marek's Disease ◽  
Marek’S Disease Virus ◽  
Marek’S Disease ◽  
Cecal Tonsil

scholarly journals Possibility to use erythrocyte antigens and feather coloration genes to determine resistance to non-plastic diseases

2020 ◽  
Vol 22 (99) ◽  
pp. 143-147
Author(s):  
L. P. Livoschenko ◽  
Y. M. Livoschenko
Keyword(s):  
Rhode Island ◽  
Tumor Regression ◽  
Marek's Disease ◽  
Neoplastic Disease ◽  
Marek’S Disease ◽  
Plumage Color ◽  
Opposite Pattern ◽  
Lymphoid Leukemia ◽  
Genetic Groups ◽  
Sarcoma Virus

Non-plastic diseases are a problem in both medical and veterinary practice. These include lymphoid leukemia (LL) and Marek's disease (CM). It should be noted that HM causes losses to poultry three times higher than LL. CM is a highly contagious viral neoplastic disease of chickens. It is known that the degree of resistance of different breeds and lines of chickens to Marek's disease (CM) and lymphoid leukemia (LL) is not the same. To date, little attention has been paid to the role of erythrocyte antigenic factors in the bird's response to morbidity. There is a relationship between the incidence among vaccinated birds and the natural susceptibility to HM birds of certain breeds and lines. The effect of protective reactions in chickens associated with erythrocyte antigenic factors in poultry selected for resistance to non-plastic diseases is still unclear. The objects of the study were chickens and 11-day-old embryos of poultry from one of the farms of Ukraine. The studies were performed on Rhode Island, Leghorn D4 and P-37 chickens. Standard strains of Rouse's sarcoma virus (HRV) were used in the study. Embryos of 11 days of incubation were infected with Rouse virus on the chorio-allantoic membrane (САМ). The results of the studies proved that the resistance to HRV had a significantly opposite correlation only with the presence of B16 antigen and the absence of X31. In chickens of the P-37 line we noted a probable difference in the number of birds of different genetic groups at loci B18 and E 8. Among birds of this line of genotypes rs and ss no individuals with locus E8 were found, while among chickens with genotype rr rarely found a bird with a locus B18. In hens of line D-4 with genotype rr, the frequency of the A12 locus was set more often than in genotypes rs and ss. As for the frequency of the B33 locus, the opposite pattern was observed. Tumor regression was probably more common in birds with antigenic factor B1 and in the absence of B33. Hypersensitivity to non-plastic diseases of chickens carrying B2, B21, B29, X50 antigens has been established. The bird, more resistant to neoplasms, had an increased number of antigens B3, B18, C26. and research in this direction continues. It is assumed that the plumage color gene (s), if present in homozygous form, is an inhibitor of sensitivity. The experiments used embryos and chickens with different plumage color: red, black, white with a yellow tinge, pure white. Their ratio is approximately 2:1:1 or 3 parts “colored” and 1 part white. It was found that among the “colored” embryos were more stable than sensitive. In fact, the resulting cleavage was close to expected.

scholarly journals Hallazgos clínico patológicos de la enfermedad de Marek en aves de combate

2019 ◽  
Vol 5 ◽  
Author(s):  
Norma Leticia Calderón Apodaca ◽  
Mayra Itzel Araujo Mayorga ◽  
Andrea Paloma Zepeda Velázquez
Keyword(s):  
Clinical Signs ◽  
Marek's Disease ◽  
Bursa Of Fabricius ◽  
Histopathological Study ◽  
Marek’S Disease ◽  
Pathological Findings ◽  
Vaccination Programs ◽  
Cell Changes ◽  
Lymphoid Infiltrates ◽  
Lymphocyte Infiltrate

Descripción de los casos. Se analizaron siete casos clínicos de doce aves de combate de diferentes edades, estos casos fueron documentados entre 2015 y 2016. El diagnóstico presuntivo fue la enfermedad de Marek, porque expresaron signos de esta enfermedadHallazgos clínicos e interpretación. Los signos clínicos fueron principalmente respiratorios, circulatorios y nerviosos. La observación histopatológica reveló cambios celulares importantes con infiltrado linfoide en diferentes tejidos, mayoritariamente en pulmón, hígado, encéfalo, nervios, intestino, riñón y bazo, con lo que se diagnosticó enfermedad de Marek.Tratamiento y evolución. Se desconoce si se aplicó tratamiento.Pruebas de laboratorio. En el estudio histopatológico, los cortes se incluyeron en formol al 10 % con tinciones de rutina. Las muestras analizadas fueron tejido perineural, encéfalo, nervio ciático braquial, pulmón, corazón, hígado, duodeno, páncreas, riñón, bazo, ciegos, bolsa de Fabricio y piel de los senos infraorbitarios. Se determinó la severidad y virulencia del virus infectante según el criterio de infiltrado linfocitario definido en las pruebas de laboratorio.Relevancia clínica. Debido a que la crianza de aves de combate se realiza en pequeña y mediana escala, y bajo métodos tradicionales, el virus de la enfermedad de Marek persiste en estas aves. Por lo tanto, se requiere el diseño y la implementación de programas especiales de vacunación, incluyendo la producción de vacunas en una presentación adecuada para pequeños avicultores. Clinical and pathological findings of Marek’s disease in fighting cocksCases report. Seven clinical cases of twelve fighting cocks of different ages, were analyzed, this cases were documented between 2015 and 2016. The presuntive diagnosis was Marek’s disease, because they expressed signs of this diseaseClinical findings. The clinical signs were mainly respiratory, circulatory and nervous. Histopathological observation revealed major cell changes with lymphoid infiltrates in different tissues, mostly in the lung, liver, brain, nerves, bowel, kidney, and spleen, leading to the diagnosis of Marek’s disease.Treatment and evolution. Whether treatment was applied is unknown.Laboratory tests. In the histopathological study, the cuts were included in 10 % formaldehyde with routine stains. The samples analyzed were perineural tissue, brain, sciatic brachial nerve, lung, heart, liver, duodenum, pancreas, kidney, spleen, blind, bursa of Fabricius and skin of infraorbital sinuses. The severity and virulence of the infecting virus was determined according to the lymphocyte infiltrate criterion defined in the laboratory tests.Clinical relevance. Because the breeding of fighting cocks is realized in small to medium scale and under traditional methods, the Marek’s disease virus persists in these birds. Therefore the design and implementation of special vaccination programs are required, including the production of vaccines in a presentation suitable for small flocks.Keywords. fighting cocks, Marek´s disease, tumor, vaccination

scholarly journals A Cell Culture System to Investigate Marek’s Disease Virus Integration into Host Chromosomes

2021 ◽  
Vol 9 (12) ◽  
pp. 2489
Author(s):  
Yu You ◽  
Tereza Vychodil ◽  
Giulia Aimola ◽  
Renato L. Previdelli ◽  
Thomas W. Göbel ◽  
...  
Keyword(s):  
Disease Virus ◽  
Marek's Disease Virus ◽  
Telomeric Repeat ◽  
Marek's Disease ◽  
Target Cells ◽  
Neoplastic Disease ◽  
Marek’S Disease Virus ◽  
Marek’S Disease ◽  
Integration Mechanism

Marek’s disease virus (MDV) is a highly oncogenic alphaherpesvirus that causes a devastating neoplastic disease in chickens. MDV has been shown to integrate its genome into the telomeres of latently infected and tumor cells, which is crucial for efficient tumor formation. Telomeric repeat arrays present at the ends of the MDV genome facilitate this integration into host telomeres; however, the integration mechanism remains poorly understood. Until now, MDV integration could only be investigated qualitatively upon infection of chickens. To shed further light on the integration mechanism, we established a quantitative integration assay using chicken T cell lines, the target cells for MDV latency and transformation. We optimized the infection conditions and assessed the establishment of latency in these T cells. The MDV genome was efficiently maintained over time, and integration was confirmed in these cells by fluorescence in situ hybridization (FISH). To assess the role of the two distinct viral telomeric repeat arrays in the integration process, we tested various knockout mutants in our in vitro integration assay. Efficient genome maintenance and integration was thereby dependent on the presence of the telomeric repeat arrays in the virus genome. Taken together, we developed and validated a novel in vitro integration assay that will shed light on the integration mechanism of this highly oncogenic virus into host telomeres.

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