Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 192
Filtrar
Mais filtros










Intervalo de ano de publicação
1.
Vet Microbiol ; 231: 214-217, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30955812

RESUMO

In this study, a recombinant ALV with ALV-K env and ALV-J backbone was generated (designated ALV-K-env-J) and tested in vitro and in vivo. The growth curve in DF1 cells showed that the recombinant virus replicated more efficiently in comparison with the ALV-J and ALV-K. Although all the infected chickens showed growth retardation compared with the non-infected chickens, the viral and serological detection showed that the positive rate and virus load detected in blood and cloaca, and the positive rate and titer of antibody against p27 from the chickens infected with ALV-K-env-J were higher than those from the chickens infected with the ALV-K, but less than those from the chickens infected with the ALV-J. All these data clearly demonstrated that the recombination event in this study increased the pathogenesis of ALV-K, and the potential recombination between different ALV subgroups should be worried when the clinical co-infections occur.


Assuntos
Vírus da Leucose Aviária/genética , Vírus da Leucose Aviária/patogenicidade , Leucose Aviária/virologia , Doenças das Aves Domésticas/virologia , Recombinação Genética , Animais , Anticorpos Antivirais/sangue , Leucose Aviária/imunologia , Galinhas/virologia , Cloaca/virologia , Doenças das Aves Domésticas/imunologia , Testes Sorológicos , Carga Viral
2.
Poult Sci ; 98(7): 2772-2780, 2019 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-30768138

RESUMO

Avian leukosis virus subgroup J has been found to infect many types of chickens with various genetic backgrounds. The ALV-J strain NX0101, which was isolated from broiler breeders in 2001, mainly induces the formation of myeloid cell tumors. However, strain HN10PY01, which was recently isolated from laying hens, mainly induces the formation of myeloid cell tumors and hemangioma. In order to determine the difference in pathogenicity of the 2 strains in broiler chickens, 2 groups of chicken embryos were infected with NA0101 and HN10PY01 separately. A comparison was made of the mortality, oncogenicity, body weights, indexes for immune organs, levels of ALV group-specific antigen p27, and mRNA expression levels of the tumor-related gene, p53, in ALV-J-infected birds and immune organs of theses chickens in response to Newcastle Disease Virus (NDV) and avian influenza virus subtype H9 (AIV-H9) vaccination. The results indicated that strain NX0101 was highly pathogenic in broiler chickens and led to a 30% mortality rate and 45% oncogenicity, compared with the HN10PY01-infected birds. Weight of chickens was also significantly lower after 15 wk (P < 0.05). In addition, the mRNA expression levels of tumor-related p53 in medulla, liver, and lung in broilers infected with strain NX0101 were significantly higher than those infected with strain HN10PY01 (P < 0.05). These results indicated that strain NX0101 had a higher replication ability in broiler chickens. The findings of this study will contribute to further elucidating the mechanisms underlying host susceptibility and tumor classification in ALV-J-infected chickens.


Assuntos
Vírus da Leucose Aviária/patogenicidade , Neoplasias/virologia , Doenças das Aves Domésticas/virologia , Virulência , Animais , Leucose Aviária/mortalidade , Leucose Aviária/patologia , Peso Corporal , Embrião de Galinha , Galinhas , Vírus da Influenza A/imunologia , Vírus da Doença de Newcastle/imunologia , Vacinas/administração & dosagem
3.
Retrovirology ; 16(1): 1, 2019 01 03.
Artigo em Inglês | MEDLINE | ID: mdl-30602379

RESUMO

BACKGROUND: The pathogenesis of immunological tolerance caused by avian leukosis virus subgroup J (ALV-J), an oncogenic retrovirus, is largely unknown. RESULTS: In this study, the development, differentiation, and immunological capability of B cells and their progenitors infected with ALV-J were studied both morphologically and functionally by using a model of ALV-J congenital infection. Compared with posthatch infection, congenital infection of ALV-J resulted in severe immunological tolerance, which was identified as the absence of detectable specific antivirus antibodies. In congenitally infected chickens, immune organs, particularly the bursa of Fabricius, were poorly developed. Moreover, IgM-and IgG-positive cells and total immunoglobulin levels were significantly decreased in these chickens. Large numbers of bursa follicles with no differentiation into cortex and medulla indicated that B cell development was arrested at the early stage. Flow cytometry analysis further confirmed that ALV-J blocked the differentiation of CD117+chB6+ B cell progenitors in the bursa of Fabricius. Furthermore, both the humoral immunity and the immunological capability of B cells and their progenitors were significantly suppressed, as assessed by (a) the antibody titres against sheep red blood cells and the Marek's disease virus attenuated serotype 1 vaccine; (b) the proliferative response of B cells against thymus-independent antigen lipopolysaccharide (LPS) in the spleen germinal centres; and (c) the capacities for proliferation, differentiation and immunoglobulin gene class-switch recombination of B cell progenitors in response to LPS and interleukin-4(IL-4) in vitro. CONCLUSIONS: These findings suggested that the anergy of B cells in congenitally infected chickens is caused by the developmental arrest and dysfunction of B cell progenitors, which is an important factor for the immunological tolerance induced by ALV-J.


Assuntos
Vírus da Leucose Aviária/imunologia , Leucose Aviária/congênito , Subpopulações de Linfócitos B/patologia , Anergia Clonal , Doenças das Aves Domésticas/congênito , Células-Tronco/patologia , Animais , Anticorpos Antivirais/sangue , Leucose Aviária/patologia , Vírus da Leucose Aviária/patogenicidade , Subpopulações de Linfócitos B/química , Subpopulações de Linfócitos B/imunologia , Subpopulações de Linfócitos B/virologia , Bolsa de Fabricius/patologia , Diferenciação Celular , Proliferação de Células , Galinhas , Citometria de Fluxo , Imunoglobulina G/sangue , Imunoglobulina M/sangue , Doenças das Aves Domésticas/patologia , Proteínas Proto-Oncogênicas c-kit/análise , Células-Tronco/química , Células-Tronco/imunologia , Células-Tronco/virologia
4.
Biosens Bioelectron ; 124-125: 1-7, 2019 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-30339973

RESUMO

A sensitive and specific photoelectrochemical (PEC) immunosensor was fabricated for subgroup J avian leukosis viruses (ALV-J) analysis based on a dual signal-on strategy. Gold nanoparticles (AuNPs) decorated graphitic carbon nitride (AuNPs/g-C3N4) as photoelectrochemical species and primary antibody (Ab1) against ALV-J were immobilized onto ITO electrode in turn. An ALP-CdTe-Ab2 bio-conjugant was fabricated by assembling second antibody (Ab2) and alkaline phosphatase (ALP) to CdTe quantum dots (QDs) surface. The PEC immunosensor was fabricated by successively anchoring the target ALV-J and ALP-CdTe-Ab2 bio-conjugants onto electrode surface via the immune recognition. By virtue of the matched energy levels between CdTe QDs and AuNPs/g-C3N4, ALP-CdTe-Ab2 bio-conjugants could serve as the PEC active probes for photocurrent enhancement. Moreover, the photocurrent response could be further enhanced attributed to the ALP catalytic chemistry to in situ produce ascorbic acid for electron donating, achieving an effective dual signal-on mode for PEC assay. On the basis of the ALV-J titers-dependent photocurrent increment, the fabricated PEC immunosensor showed high sensitivity, specificity and stability for ALV-J assay in a wide linear range with a low detection limit of 85 TCID50/mL. This PEC immunosensor with the dual signal-on strategy may open up a promising platform for more target analytes in novel immune analysis and clinical diagnostics.


Assuntos
Vírus da Leucose Aviária/isolamento & purificação , Leucose Aviária/diagnóstico , Técnicas Biossensoriais , Técnicas Eletroquímicas , Fosfatase Alcalina/química , Fosfatase Alcalina/imunologia , Animais , Leucose Aviária/virologia , Vírus da Leucose Aviária/patogenicidade , Compostos de Cádmio/química , Elétrons , Ouro/química , Grafite/química , Imunoensaio , Limite de Detecção , Nanopartículas Metálicas/química , Compostos de Nitrogênio/química , Pontos Quânticos/química , Telúrio/química
5.
Viruses ; 10(5)2018 05 18.
Artigo em Inglês | MEDLINE | ID: mdl-29783672

RESUMO

Superinfection of Marek's disease virus (MDV) and avian leukosis virus subgroup J (ALV-J) causes lethal neoplasia and death in chickens. However, whether there is synergism between the two viruses in viral replication and pathogenicity has remained elusive. In this study, we found that the superinfection of MDV and ALV-J increased the viral replication of the two viruses in RNA and protein level, and synergistically promoted the expression of IL-10, IL-6, and TGF-ß in chicken embryo fibroblasts (CEF). Moreover, MDV and ALV-J protein expression in dual-infected cells detected by confocal laser scanning microscope appeared earlier in the cytoplasm and the nucleus, and caused more severe cytopathy than single infection, suggesting that synergistically increased MDV and ALV-J viral-protein biosynthesis is responsible for the severe cytopathy. In vivo, compared to the single virus infected chickens, the mortality and tumor formation rates increased significantly in MDV and ALV-J dual-infected chickens. Viral loads of MDV and ALV-J in tissues of dual-infected chickens were significantly higher than those of single-infected chickens. Histopathology observation showed that more severe inflammation and tumor cells metastases were present in dual-infected chickens. In the present study, we concluded that synergistic viral replication of MDV and ALV-J is responsible for the enhanced pathogenicity in superinfection of chickens.


Assuntos
Vírus da Leucose Aviária/patogenicidade , Mardivirus/patogenicidade , Superinfecção/virologia , Animais , Leucose Aviária/virologia , Vírus da Leucose Aviária/fisiologia , Galinhas/virologia , Mediadores da Inflamação/metabolismo , Mardivirus/fisiologia , Doença de Marek/virologia , Carga Viral , Virulência , Replicação Viral
6.
Viruses ; 10(4)2018 04 13.
Artigo em Inglês | MEDLINE | ID: mdl-29652854

RESUMO

In recent years, cases of avian leukosis virus (ALV) infection have become more frequent in China. We isolated 6 ALV strains from yellow feather broiler breeders in south China from 2014 to 2016. Their full genomes were sequenced, compared, and analyzed with other reference strains of ALV. The complete genomic nucleotide sequences of GD150509, GD160403, GD160607, GDFX0601, and GDFX0602 were 7482 bp in length, whereas GDFX0603 was 7480 bp. They shared 99.7% to 99.8% identity with each other. Homology analysis showed that the gag, pol, long terminal repeats (LTRs), and the transmembrane region (gp37) of the env genes of the 6 viruses were well conserved to endogenous counterpart sequences (>97.8%). However, the gp85 genes displayed high variability with any known chicken ALV strains. Growth kinetics of DF-1 cells infected with the isolated ALV showed viral titers that were lower than those infected with the GD13 (ALV-A), CD08 (ALV-B), and CHN06 (ALV-J) on day 7 post-infection. The infected Specific-pathogen-free (SPF) chickens could produce continuous viremia, atrophy of immune organs, growth retardation and no tumors were observed. These subgroup ALVs are unique and may be common in south China. The results suggested that updating the control and eradication program of exogenous ALV for yellow feather broiler breeders in south China needs to be considered because of the emergence of the new subgroup viruses.


Assuntos
Vírus da Leucose Aviária/genética , Vírus da Leucose Aviária/patogenicidade , Leucose Aviária/virologia , Variação Genética , Filogenia , Recombinação Genética , Animais , Leucose Aviária/patologia , Vírus da Leucose Aviária/classificação , Vírus da Leucose Aviária/isolamento & purificação , Galinhas , China , Genoma Viral , Homologia de Sequência , Sequências Repetidas Terminais , Proteínas Virais/genética , Sequenciamento Completo do Genoma
7.
In Vitro Cell Dev Biol Anim ; 54(1): 41-51, 2018 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-29197030

RESUMO

Avian leukemia subgroup J (ALV-J) is one of the most detrimental neoplastic diseases in poultry production. However, the differences between somatic cells and immune cells post-infection remain poorly understood. The aim of our study was to detect the different responses in chicken to infection with ALV-J in different cell lines. In this study, we detected transcriptome expression changes during infection with ALV-J in chicken embryo fibroblast (CEF) and HD11 cell lines. RNA-Seq was used to determine the expression levels of mRNA transcripts from the two cell types after infection with ALV-J at 1, 4, and 7 dpi, and gene ontology analyses were used to cluster differentially expressed genes into pathways. Quantitative real-time PCR confirmed the expression of 336 and 269 differentially expressed genes in CEF and HD11 lines, respectively, involved in innate immunity (OASL, CCL4), adaptive immunity (LYZ, CD72), apoptosis and autophagy (WISP2, COMP), inflammation (JSC, IL8), and tumorgenesis (PCNA, GPX3). The notable signal transduction pathways included the PPARs signaling pathway and ECM-receptor interactions in CEF, and the Toll-like receptor, NOD-like receptor, and RIG-I-like receptor signaling pathways in HD11. To our knowledge, this is the first study to use high-throughput sequencing methods to investigate viral infection in different cell types. The results of the present study form a foundation for developing potential biological markers for viral infection.


Assuntos
Vírus da Leucose Aviária/patogenicidade , Leucose Aviária/genética , Galinhas/virologia , Interações Hospedeiro-Patógeno/genética , Imunidade Adaptativa/genética , Animais , Apoptose/genética , Autofagia/genética , Leucose Aviária/imunologia , Linhagem Celular , Embrião de Galinha , Galinhas/genética , Regulação da Expressão Gênica , Ontologia Genética , Interações Hospedeiro-Patógeno/imunologia , Imunidade Inata/genética , Transdução de Sinais/genética , Replicação Viral
8.
Microb Pathog ; 112: 142-147, 2017 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-28916320

RESUMO

J subgroup avian leukosis virus (ALV-J) is an exogenous retrovirus of avian. A key feature of ALV-J infection is leading to severe immunosuppressive characteristic of diseases. Viral components of retrovirus were reported closely associated with immunosuppression, and several similarities between exosomes and retrovirus preparations have lead to the hypotheses of retrovirus hijacker exosomes pathway. In this study, we purified exosomes from DF-1 cells infected and uninfected by ALV-J. Electron microscopy and mass spectrometry (MS) analysis showed that ALV-J not only increased the production of exosomes from ALV-J infected DF-1 cells (Exo-J) but also stimulated some proteins expression, especially ALV-J components secreted in exosomes. Immunosuppressive domain peptide (ISD) of envelope subunit transmembrane (TM) and gag of ALV-J were secreted in Exo-J. It has been reported that HIV gag was budded from endosome-like domains of the T cell plasma membrane. But env protein was first detected in exosomes from retrovirus infected cells. We found that Exo-J caused negative effects on splenocytes in a dose-dependant manner by flow cytometric analysis. And low dose of Exo-J activated immune activity of splenocytes, while high dose possessed immunosuppressive properties. Interestingly, Exo-J has no significant effects on the immunosuppression induced by ALV-J, and the immunosuppressive effects induced by Exo-J lower than that by ALV-J. Taken together, our data indicated that Exo-J supplied a microenvironment for the replication and transformation of ALV-J.


Assuntos
Vírus da Leucose Aviária/fisiologia , Leucose Aviária/virologia , Exossomos/metabolismo , Produtos do Gene env/metabolismo , Produtos do Gene gag/metabolismo , Animais , Vírus da Leucose Aviária/patogenicidade , Linhagem Celular , Galinhas , Interações Hospedeiro-Patógeno , Imunossupressão , Microscopia Eletrônica de Transmissão
9.
Oncotarget ; 8(21): 34961-34970, 2017 May 23.
Artigo em Inglês | MEDLINE | ID: mdl-28415618

RESUMO

Avian leukosis virus subgroup (ALV-J) is an oncogenic neoplasm-inducing retrovirus that causes significant economic losses in the poultry industry. Recent studies have demonstrated circular RNAs (circRNAs) are implicated in pathogenic processes; however, no research has indicated circRNAs are involved in resistance to disease. In this study, over 1800 circRNAs were detected by circRNA sequencing of liver tissues from ALV-J-resistant (n = 3) and ALV-J-susceptible chickens (n = 3). 32 differentially expressed circRNAs were selected for analyzing including 12 upregulated in ALV-J-resistant chickens and 20 upregulated in ALV-J-susceptible chickens, besides, the top five microRNAs (miRNAs) for 12 upregulated circRNAs in ALV-J-resistant chickens were analyzed. Gene ontology and KEGG pathway analyses were performed for miRNA target genes, the predicted genes were mainly involved in immune pathways. This study provides the first evidence that circRNA alterations are involved in resistance to ALV-J-induced tumor formation. We propose circRNAs may help to mediate tumor induction and development in chickens.


Assuntos
Galinhas/genética , Resistência à Doença , RNA/genética , Animais , Leucose Aviária/genética , Vírus da Leucose Aviária/genética , Vírus da Leucose Aviária/patogenicidade , Regulação Neoplásica da Expressão Gênica , Fígado/virologia , Doenças das Aves Domésticas/genética , Doenças das Aves Domésticas/virologia , Análise de Sequência de RNA/veterinária , Regulação para Cima
10.
Oncotarget ; 7(49): 80275-80287, 2016 Dec 06.
Artigo em Inglês | MEDLINE | ID: mdl-27852059

RESUMO

Avian leukosis virus subgroup J (ALV-J) is an oncogenic virus causing hemangiomas and myeloid tumors in chickens. Interleukin-6 (IL-6) is a multifunctional pro-inflammatory interleukin involved in many types of cancer. We previously demonstrated that IL-6 expression was induced following ALV-J infection in chickens. The aim of this study is to characterize the mechanism by which ALV-J induces IL-6 expression, and the role of IL-6 in tumor development. Our results demonstrate that ALV-J infection increases IL-6 expression in chicken splenocytes, peripheral blood lymphocytes, and vascular endothelial cells. IL-6 production is induced by the ALV-J envelope protein gp85 and capsid protein p27 via PI3K- and NF-κB-mediated signaling. IL-6 in turn induced expression of vascular endothelial growth factor (VEGF)-A and its receptor, VEGFR-2, in vascular endothelial cells and embryonic vascular tissues. Suppression of IL-6 using siRNA inhibited the ALV-J induced VEGF-A and VEGFR-2 expression in vascular endothelial cells, indicating that the ALV-J-induced VEGF-A/VEGFR-2 expression is mediated by IL-6. As VEGF-A and VEGFR-2 are important factors in oncogenesis, our findings suggest that ALV-J hijacks IL-6 to promote tumorigenesis, and indicate that IL-6 could potentially serve as a therapeutic target in ALV-J infections.


Assuntos
Vírus da Leucose Aviária/metabolismo , Leucose Aviária/enzimologia , Células Endoteliais/enzimologia , Interleucina-6/metabolismo , NF-kappa B/metabolismo , Fosfatidilinositol 3-Quinase/metabolismo , Baço/enzimologia , Fator A de Crescimento do Endotélio Vascular/metabolismo , Animais , Leucose Aviária/genética , Leucose Aviária/virologia , Vírus da Leucose Aviária/genética , Vírus da Leucose Aviária/patogenicidade , Proteínas do Capsídeo/genética , Proteínas do Capsídeo/metabolismo , Transformação Celular Viral , Células Cultivadas , Galinhas , Células Endoteliais/virologia , Interações Hospedeiro-Patógeno , Interleucina-6/genética , Fator de Transcrição STAT3/genética , Fator de Transcrição STAT3/metabolismo , Transdução de Sinais , Baço/virologia , Fatores de Tempo , Transfecção , Fator A de Crescimento do Endotélio Vascular/genética , Receptor 2 de Fatores de Crescimento do Endotélio Vascular/genética , Receptor 2 de Fatores de Crescimento do Endotélio Vascular/metabolismo , Proteínas do Envelope Viral/genética , Proteínas do Envelope Viral/metabolismo
11.
Arch Virol ; 161(12): 3473-3481, 2016 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-27654667

RESUMO

In our previous study, six subgroup J strains of avian leukosis virus (ALV-J)-associated acutely transforming viruses carrying different lengths of the v-fps oncogene, designated as Fu-J and Fu-J1-5, were isolated and characterized from fibrosarcomas in ALV-J-infected chickens. In the present study, the oncogenic potential of Fu-J and Fu-J1-5 was investigated using a reverse genetics technique. Six replication-defective viruses, named rFu-J and rFu-J1-5, were rescued with the replication-competent rescued ALV-J strain rSDAU1005 as a helper virus by co-transfection of chicken embryo fibroblast monolayers with infectious clone plasmids. Experimental bird studies were performed, demonstrating that only the rescued rFu-J virus carrying the complete v-fps oncogene with rSDAU1005 as the helper virus could induce acute fibrosarcoma after inoculation in specific-pathogen-free (SPF) chickens. These results provide direct evidence that the replication-defective acutely transforming Fu-J virus, with the complete v-fps oncogene, was associated with acute fibrosarcoma in chickens infected with ALV-J in the field, as reported previously.


Assuntos
Vírus da Leucose Aviária/genética , Vírus da Leucose Aviária/isolamento & purificação , Fibrossarcoma/veterinária , Proteínas Oncogênicas/genética , Doenças das Aves Domésticas/patologia , Doenças das Aves Domésticas/virologia , Experimentação Animal , Animais , Vírus da Leucose Aviária/patogenicidade , Testes de Carcinogenicidade , Galinhas , Fibrossarcoma/virologia , Vírus Auxiliares , Organismos Livres de Patógenos Específicos , Replicação Viral
12.
Vet Immunol Immunopathol ; 177: 42-7, 2016 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-27436443

RESUMO

To investigate the effects of co-infections of subgroup J avian leukosis virus (ALV-J) and Eimeria tenella on the pathogenesis in specific-pathogen-free (SPF) white leghorn chickens, groups of chickens were infected with ALV-J strain NX0101 at one day of age or with E. tenella at 14 days of age or both. The control group was left uninfected and was mock-inoculated with phosphate buffer saline (PBS). Mortality rates, body weights, cecal lesions, and viremia of infected chickens in each group were evaluated. Immune status was evaluated by measuring several parameters: immune organ weight/body weight index, specific humoral responses to inactivated NDV vaccine and to inoculated E. tenella, proportions of blood CD3+CD4+ and CD3+CD8α+ lymphocytes and transcriptional levels of cytokines in blood and cecal tonsils. The results show that co-infections of ALV-J and E. tenella induced a higher mortality rate and a lower body weight in SPF chickens compared to single-pathogen infection. In co-infected chickens, ALV-J accelerated the disease symptoms induced by E. tenella, and the E. tenella extended the ALV-J viremia. Thymus atrophy, decrease in the humoral response levels to pathogens and the NDV vaccine, modifications in the blood lymphocyte sub-populations and transcriptional cytokine disorders were found in co-infected chickens compared to chickens infected with one pathogen alone and to controls. We underline a synergy between ALV-J and E. tenella that results in increasing pathogenesis in SPF chickens.


Assuntos
Vírus da Leucose Aviária/imunologia , Vírus da Leucose Aviária/patogenicidade , Galinhas/imunologia , Eimeria tenella/imunologia , Eimeria tenella/patogenicidade , Animais , Animais Recém-Nascidos , Leucose Aviária/etiologia , Vírus da Leucose Aviária/classificação , Galinhas/parasitologia , Galinhas/virologia , Coccidiose/etiologia , Coccidiose/veterinária , Coinfecção/etiologia , Coinfecção/veterinária , Citocinas/genética , Imunidade Celular/genética , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Organismos Livres de Patógenos Específicos , Virulência
13.
Infect Genet Evol ; 44: 130-136, 2016 10.
Artigo em Inglês | MEDLINE | ID: mdl-27349993

RESUMO

Subgroup J avian leukosis virus (ALV-J) is an oncogenic retrovirus known to induce tumor formation and immunosuppression in infected chickens. One of the organs susceptible to ALV-J is the bone marrow, from which specialized antigen-presenting cells named dendritic cells (BM-DCs) are derived. Notably, these cells possess the unique ability to induce primary immune responses. In the present study, a method of cultivating and purifying DCs from chicken bone marrow in vitro was established to investigate the effects of ALV-J infection on BM-DC differentiation or generation. The results indicated that ALV-J not only infects the chicken bone marrow mononuclear cells but also appears to inhibit the differentiation and maturation of BM-DCs and to trigger apoptosis. Moreover, substantial reductions in the mRNA expression of TLR1, TLR2, TLR3, MHCI, and MHCII and in cytokine production were detected in the surviving BM-DCs following ALV-J infection. These findings indicate that ALV-J infection disrupts the process of bone marrow mononuclear cell differentiation into BM-DCs likely via altered antigen presentation, resulting in a downstream immune response in affected chickens.


Assuntos
Vírus da Leucose Aviária/patogenicidade , Leucose Aviária/patologia , Leucose Aviária/virologia , Monócitos/virologia , Animais , Apoptose , Diferenciação Celular , Células Cultivadas , Galinhas/virologia , Citocinas/genética , Citocinas/metabolismo , Células Dendríticas/virologia , Interações Hospedeiro-Patógeno , Monócitos/patologia , Doenças das Aves Domésticas/virologia , Receptores Toll-Like/genética , Receptores Toll-Like/metabolismo
14.
Virus Genes ; 52(3): 365-71, 2016 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-27108997

RESUMO

Transduction of oncogenes by ALVs and generation of acute transforming viruses is common in natural viral infections. In order to understand the molecular basis for the rapid oncogenicity of Fu-J, an acutely transforming avian leukosis virus isolated from fibrosarcomas in crossbreed broilers infected with subgroup J avian leukosis virus (ALV-J) in China, complete genomic structure of Fu-J virus was determined by PCR amplification and compared with those of Fu-J1, Fu-J2, Fu-J3, Fu-J4, and Fu-J5 reported previously. The results showed that the genome of Fu-J was defective, with parts of gag gene replaced by the complete v-fps oncogene and encoded a 137 kDa Gag-fps fusion protein. Sequence analysis revealed that Fu-J and Fu-J1 to Fu-J5 were related quasi-species variants carrying different lengths of v-fps oncogenes generated from recombination between helper virus and c-fps gene. Comparison of virus carrying v-fps oncogene also gave us a glimpse of the molecular characterization and evolution process of the acutely transforming ALV.


Assuntos
Vírus da Leucose Aviária/genética , Leucose Aviária/virologia , Proteínas de Fusão gag-onc/genética , Proteínas Oncogênicas/genética , Vírus Oncogênicos/genética , Doenças das Aves Domésticas/virologia , Proteínas Tirosina Quinases/genética , Animais , Vírus da Leucose Aviária/isolamento & purificação , Vírus da Leucose Aviária/patogenicidade , Vírus do Sarcoma Aviário/genética , Sequência de Bases , Embrião de Galinha , Galinhas/virologia , DNA Viral , Fibrossarcoma/virologia , Produtos do Gene gag/genética , Genes Virais , Vírus Auxiliares/genética , Retroviridae/genética , Replicação Viral
15.
Arch Virol ; 161(6): 1623-32, 2016 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-27016933

RESUMO

Endogenous retroviruses (ERVs) are important retroelements that reside in host genomes. However, ERV expression patterns and regulatory mechanisms are poorly understood. In this study, chicken embryo fibroblasts (CEFs) and MSB1 cells infected with Marek's disease virus (MDV) exhibited significantly increased expression of env from the endogenous retrovirus ALVE. In contrast, env expression was significantly lower in CEF and MSB1 cells infected with exogenous avian leukosis virus J (ALVJ) at the early infection stage. Furthermore, env was found to be ubiquitously expressed in various chicken tissues, with high expression in certain tissues at 2 days of age and low levels in most tissues, including immune organs (thymus, spleen and bursa) as well as the brain and heart, at 35 days of age. Sequence analysis revealed miR-155 target sites in env transcripts, which was verified using a firefly luciferase reporter assay, and treatment with miR-155 agomir significantly decreased levels of env transcripts in MSB1 and CEF cells. Together, these findings suggest that the env gene from the endogenous retrovirus ALVE is regulated by miR-155.


Assuntos
Retrovirus Endógenos/genética , Genes env , MicroRNAs/genética , Animais , Leucose Aviária/virologia , Vírus da Leucose Aviária/genética , Vírus da Leucose Aviária/patogenicidade , Células Cultivadas , Embrião de Galinha , Galinhas , Retrovirus Endógenos/classificação , Retrovirus Endógenos/patogenicidade , Regulação Viral da Expressão Gênica , Mardivirus/genética , Mardivirus/patogenicidade , Filogenia
16.
Virus Res ; 215: 65-71, 2016 Apr 02.
Artigo em Inglês | MEDLINE | ID: mdl-26811903

RESUMO

Many pathogens trigger caspase-1-mediated innate immune responses. Avian leukosis virus subgroup J (ALV-J) causes serious immunosuppression and diverse tumors in chicks. The caspase-1 inflammasome mechanism of response to ALV-J invading remains unclear. Here we investigated the expression of caspase-1, the inflammasome adaptor NLRP3, IL-1ß and IL-18 in response to ALV-J infection in the liver of chick. We found caspase-1 mRNA expression was elevated at 5 dpi and peaked at 7 dpi in ALV-J infected animals. Corresponding to this, the expressions of NLRP3 and proinflammatory cytokines IL-1ß and IL-18 were significantly increased at 5 or 7 dpi. In addition, caspase-1 protein expression and inflammatory cell infiltration were induced after virus infection. These results indicated that ALV-J infection could trigger the caspase-1- mediated inflammatory response in chicks. Thus, an understanding of the inflammatory responses can provide a better insight into the pathogenicity of ALV-J and a possible anti-virus target for ALV-J infection.


Assuntos
Vírus da Leucose Aviária/patogenicidade , Caspase 1/análise , Genótipo , Inflamação/patologia , Fígado/patologia , Animais , Vírus da Leucose Aviária/genética , Perfilação da Expressão Gênica , Interleucina-18/análise , Interleucina-1beta/análise , Proteína 3 que Contém Domínio de Pirina da Família NLR/análise , RNA Mensageiro/análise , Fatores de Tempo
17.
Avian Pathol ; 44(1): 43-9, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-25484188

RESUMO

To study interactions between avian leukosis virus subgroup J (ALV-J) and reticuloendotheliosis virus (REV) and the effects of co-infection on pathogenicity of these viruses, 1-day-old broiler chicks were infected with ALV-J, REV or both ALV-J and REV. The results indicated that co-infection of ALV-J and REV induced more growth retardation and higher mortality rate than ALV-J or REV single infection (P < 0.05). Chickens co-infected with ALV-J and REV also showed more severe immunosuppression than those with a single infection. This was manifested by significantly lower bursa of Fabricius and thymus to body weight ratios and lower antibody responses to Newcastle disease virus and H9-avian influenza virus (P < 0.05). Perihepatitis and pericarditis related to severe infection with Escherichia coli were found in many of the dead birds. E. coli was isolated from each case of perihepatitis and pericarditis. The mortality associated with E. coli infection in the co-infection groups was significantly higher than in the other groups (P < 0.05). Among 516 tested E. coli isolates from 58 dead birds, 12 serotypes of the O-antigen were identified in two experiments. Different serotypes of E. coli strains were even isolated from the same organ of the same bird. Diversification of O-serotypes suggested that perihepatitis and pericarditis associated with E. coli infection was the most frequent secondary infection following the immunosuppression induced by ALV-J and REV co-infection. These results suggested that the co-infection of ALV-J and REV caused more serious synergistic pathogenic effects, growth retardation, immunosuppression, and secondary E. coli infection in broiler chickens.


Assuntos
Vírus da Leucose Aviária/patogenicidade , Galinhas , Coinfecção/veterinária , Escherichia coli/patogenicidade , Doenças das Aves Domésticas/fisiopatologia , Doenças das Aves Domésticas/virologia , Vírus da Reticuloendoteliose Aviária/patogenicidade , Animais , Bolsa de Fabricius/patologia , Coinfecção/microbiologia , Coinfecção/mortalidade , Coinfecção/fisiopatologia , Coinfecção/virologia , Imunossupressão/veterinária , Doenças das Aves Domésticas/microbiologia , Doenças das Aves Domésticas/mortalidade , Sorotipagem/veterinária , Timo/patologia
18.
Vet Pathol ; 52(6): 1052-6, 2015 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-25445321

RESUMO

To investigate the molecular mechanisms of the oncogenic effects of avian leukosis virus subgroup J (ALV-J), we examined mutations in and the expression of p53 in the myelocytomas distributed in the liver, spleen, trachea, and bone marrow, as well as in fibrosarcomas in the abdominal cavity and hemangiomas in skin from chickens that were naturally or experimentally infected with ALV-J. Two types of mutations in the p53 gene were detected in myelocytomas of both the experimentally infected and the naturally infected chickens and included point mutations and deletions. Two of the point mutations have not been reported previously. Partial complementary DNA clones with a 122-bp deletion in the p53 gene ORF and a 15-bp deletion in the C-terminus were identified in the myelocytomas. In addition, moderate expression of the mutant p53 protein was detected in the myelocytomas that were distributed in the liver, trachea, spleen, and bone marrow. Mutant p53 protein was not detected in the subcutaneous hemangiomas or in the abdominal fibrosarcomas associated with natural and experimental ALV-J infection, respectively. These results identify mutations associated with abnormal expression of p53 in ALV-J-associated myelocytomas, suggesting a role in tumorigenesis.


Assuntos
Vírus da Leucose Aviária/patogenicidade , Leucose Aviária/complicações , Galinhas/virologia , Hemangioma/veterinária , Doenças das Aves Domésticas/patologia , Proteína Supressora de Tumor p53/genética , Animais , Leucose Aviária/virologia , Vírus da Leucose Aviária/isolamento & purificação , Feminino , Hemangioma/patologia , Mutação , Doenças das Aves Domésticas/virologia , Organismos Livres de Patógenos Específicos
19.
PLoS One ; 9(1): e86546, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-24466146

RESUMO

Epidemiological studies suggest that retroviruses, including human immunodeficiency virus type 1, are associated with cardiomyopathy and myocarditis, but a causal relationship remains to be established. We encountered unusual cardiomyocyte hypertrophy and mitosis in Japanese native fowls infected with subgroup A of the avian leukosis viruses (ALVs-A), which belong to the genus Alpharetrovirus of the family Retroviridae and mainly induce lymphoid neoplasm in chickens. The affected hearts were evaluated by histopathology and immunohistochemistry, viral isolation, viral genome sequencing and experimental infection. There was non-suppurative myocarditis in eighteen fowls and seven of them had abnormal cardiomyocytes, which were distributed predominantly in the left ventricular wall and showed hypertrophic cytoplasm and atypical large nuclei. Nuclear chains and mitosis were frequently noted in these cardiomyocytes and immunohistochemistry for proliferating cell nuclear antigen supported the enhancement of mitotic activity. ALVs were isolated from all affected cases and phylogenic analysis of envSU genes showed that the isolates were mainly classified into two different clusters, suggesting viral genome diversity. In ovo experimental infection with two of the isolates was demonstrated to cause myocarditis and cardiomyocyte hypertrophy similar to those in the naturally occurring lesions and cardiac hamartoma (rhabdomyoma) in a shorter period of time (at 70 days of age) than expected. These results indicate that ALVs cause myocarditis as well as cardiomyocyte abnormality in chickens, implying a pathogenetic mechanism different from insertional mutagenesis and the existence of retrovirus-induced heart disorder.


Assuntos
Vírus da Leucose Aviária/patogenicidade , Leucose Aviária/virologia , Cardiomegalia/veterinária , Miocardite/veterinária , Doenças das Aves Domésticas/epidemiologia , Rabdomioma/veterinária , Animais , Leucose Aviária/complicações , Leucose Aviária/patologia , Vírus da Leucose Aviária/genética , Vírus da Leucose Aviária/isolamento & purificação , Cardiomegalia/patologia , Cardiomegalia/virologia , Galinhas/virologia , DNA Viral/genética , Genoma Viral , Humanos , Técnicas Imunoenzimáticas , Epidemiologia Molecular , Miocardite/patologia , Miocardite/virologia , Filogenia , Reação em Cadeia da Polimerase , Doenças das Aves Domésticas/etiologia , Rabdomioma/patologia , Rabdomioma/virologia , Replicação Viral
20.
PLoS One ; 9(1): e84797, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-24465434

RESUMO

Subgroup J avian leukosis virus (ALV-J) was first isolated from meat-type chickens that had developed myeloid leukosis and since 2008, ALV-J infections in chickens have become widespread in China. A comparison of the sequence of ALV-J epidemic isolates with HPRS-103, the ALV-J prototype virus, revealed several distinct features, one of which is a 19-nucleotide (nt) insertion in the leader sequence. To determine the role of the 19-nt insertion in ALV-J pathogenicity, a pair of viruses were constructed and rescued. The first virus was an ALV-J Chinese isolate (designated rSD1009) containing the 19-nt insertion in its leader sequence. The second virus was a clone, in which the leader sequence had a deleted 19-nt sequence (designated rSD1009△19). Compared with rSD1009△19, rSD1009 displayed a moderate growth advantage in vitro. However, no differences were demonstrated in either viral replication or oncogenicity between the two rescued viruses in chickens. These results indicated that the 19-nt insertion contributed to ALV-J replication in vitro but was not related to its pathogenicity in vivo.


Assuntos
Vírus da Leucose Aviária/metabolismo , Vírus da Leucose Aviária/patogenicidade , Proteínas Virais/fisiologia , Animais , Leucose Aviária/virologia , Vírus da Leucose Aviária/genética , Linhagem Celular , Galinhas , Doenças das Aves Domésticas/virologia , Proteínas Virais/genética , Virulência/genética , Virulência/fisiologia , Replicação Viral/genética , Replicação Viral/fisiologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA