Differences in pathogenicity among strains of the same or different avian leukosis virus subgroups

Průková, Dana; Vernerová, Zdeňka; Pilčı́k, Tomáš; Stepanets,; Indrová, M; Geryk, Josef; Plachý, Jiřı́; Hejnar, Jiřı́; Svoboda, Jan

doi:10.1080/03079450601102921

Cited by 9 publications

(6 citation statements)

References 44 publications

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“…In many studies on ALV-J pathogenicity, immune tissue injury was deemed the major reason for immunosuppression 38 39 . In the present study, ALV-J was shown to influence the differentiation of DCs and to induce apoptosis though the aberrant expression of miRNAs in vitro .…”

Section: Discussionmentioning

confidence: 99%

Subgroup J avian leukosis virus infection of chicken dendritic cells induces apoptosis via the aberrant expression of microRNAs

Liu

Dai

et al. 2016

Sci Rep

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Subgroup J avian leukosis virus (ALV-J) is an oncogenic retrovirus that causes immunosuppression and enhances susceptibility to secondary infection. The innate immune system is the first line of defense in preventing bacterial and viral infections, and dendritic cells (DCs) play important roles in innate immunity. Because bone marrow is an organ that is susceptible to ALV-J, the virus may influence the generation of bone marrow-derived DCs. In this study, DCs cultured in vitro were used to investigate the effects of ALV infection. The results revealed that ALV-J could infect these cells during the early stages of differentiation, and infection of DCs with ALV-J resulted in apoptosis. miRNA sequencing data of uninfected and infected DCs revealed 122 differentially expressed miRNAs, with 115 demonstrating upregulation after ALV-J infection and the other 7 showing significant downregulation. The miRNAs that exhibited the highest levels of upregulation may suppress nutrient processing and metabolic function. These results indicated that ALV-J infection of chicken DCs could induce apoptosis via aberrant microRNA expression. These results provide a solid foundation for the further study of epigenetic influences on ALV-J-induced immunosuppression.

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Section: Discussionmentioning

confidence: 99%

Subgroup J avian leukosis virus infection of chicken dendritic cells induces apoptosis via the aberrant expression of microRNAs

Liu

Dai

et al. 2016

Sci Rep

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“…Like ts1, other cytopathic retroviruses, including HIV-1, SIV and FIV, cause damage to thymic cytoarchitecture and loss of thymocytes in their respective host species, making the thymus unable to supply naïve T cells for protective immune responses to viral variants as they appear during the disease course [8][9][10]13,[63][64][65]. HAART therapies, like those currently in use for treatment of HIV-AIDS, may not restore thymopoiesis even assuming that normal Tprogenitor cells are produced and sent to the thymus from the bone marrow in these patients [66].…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, although HIV-1 and the lentivirus simian immunodeficiency virus (SIV) use CD4 as their surface receptor on T cells, other T cell-tropic retroviruses do not [5][6][7]. Despite this, thymic atrophy, selective infection and killing of CD4+ T-lineage cells, or neoplastic transformation of thymocytes, are common characteristics of diseases caused by these viral agents [8][9][10][11][12][13][14]. At present, the cause of T cell death after infection by these viruses is unknown.…”

Section: Introductionmentioning

confidence: 99%

The drug monosodium luminol (GVT®) preserves thymic epithelial cell cytoarchitecture and allows thymocyte survival in mice infected with the T cell-tropic, cytopathic retrovirus ts1

et al. 2009

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“…Aside from experimental techniques, ALVs are transmitted by three methods: horizontal (direct or indirect contact); vertical (congenital from female to offspring); and genetic (viral genome transmission from parent) (Pruková et al, ). Quantities of ALVs are shed by both oral and cloacal routes, with the highest viral concentration in faeces; exposed skin is the portal of entry most conducive to infection (Weyl & Dougherty, ).…”

Section: Avian Leucosis Virusesmentioning

confidence: 99%

Human‐Aided Movement of Viral Disease and the Archaeology of Avian Osteopetrosis

Fothergill

2017

Intl J of Osteoarchaeology

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The term avian osteopetrosis is used to describe alterations to the skeletal elements of several species of domestic bird, most typically the chicken, Gallus gallus domesticus (L. 1758). Such lesions are routinely identified in animal bones from archaeological sites due to their distinctive appearance, which is characterised by proliferative diaphyseal thickening. These lesions are relatively uncomplicated for specialists to differentially diagnose and are caused by a range of avian leucosis viruses in a series of subgroups. Only some avian leucosis viruses cause the development of such characteristic lesions in osteological tissue. Viraemia is necessary for the formation of skeletal pathology, and avian osteopetrosis lesions affect skeletal elements at different rates. Lesion expression differs by the age and sex of the infected individual, and environmental conditions have an impact on the prevalence of avian leucosis viruses in poultry flocks. These factors have implications for the ways in which diagnosed instances of avian osteopetrosis in archaeological assemblages are interpreted. By integrating veterinary research with archaeological evidence for the presence of avian leucosis viruses across Western Europe, this paper discusses the nature of these pathogens, outlines criteria for differential diagnosis, and offers a fresh perspective on the human‐aided movement of animal disease in the past through investigation of the incidence and geographic distribution of avian osteopetrosis lesions from the first century BC to the post‐medieval period. © 2017 The Authors International Journal of Osteoarchaeology Published by John Wiley & Sons Ltd.

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Differences in pathogenicity among strains of the same or different avian leukosis virus subgroups

Cited by 9 publications

References 44 publications

Subgroup J avian leukosis virus infection of chicken dendritic cells induces apoptosis via the aberrant expression of microRNAs

Subgroup J avian leukosis virus infection of chicken dendritic cells induces apoptosis via the aberrant expression of microRNAs

The drug monosodium luminol (GVT®) preserves thymic epithelial cell cytoarchitecture and allows thymocyte survival in mice infected with the T cell-tropic, cytopathic retrovirus ts1

Human‐Aided Movement of Viral Disease and the Archaeology of Avian Osteopetrosis

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