Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
Add more filters










Database
Language
Publication year range
1.
Infect Genet Evol ; 60: 48-57, 2018 06.
Article in English | MEDLINE | ID: mdl-29409800

ABSTRACT

Infectious bursal disease (IBD) is an immunosuppressive viral disease, present worldwide, which causes mortality and immunosuppression in young chickens. The causative agent, the Avibirnavirus IBDV, is a non-enveloped virus whose genome consists of two segments (A and B) of double-stranded RNA. Different pathotypes of IBDV exist, ranging from attenuated vaccine strains to very virulent viruses (vvIBDV). In Algeria, despite the prophylactic measures implemented, cases of IBD are still often diagnosed clinically and the current molecular epidemiology of IBDV remains unknown. The presence of the virus and especially of strains genetically close to vvIBDV was confirmed in 2000 by an unpublished OIE report. In this study, nineteen IBDV isolates were collected in Algeria between September 2014 and September 2015 during clinical outbreaks. These isolates were analyzed at the genetic, antigenic and pathogenic levels. Our results reveal a broad genetic and phenotypic diversity of pathogenic IBDV strains in Algeria, with, i) the circulation of viruses with both genome segments related to European vvIBDV, which proved as pathogenic for specific pathogen-free chickens as vvIBDV reference strain, ii) the circulation of viruses closely related - yet with a specific segment B - to European vvIBDV, their pathogenicity being lower than reference vvIBDV, iii) the detection of reassortant viruses whose segment A was related to vvIBDV whereas their segment B did not appear closely related to any reference sequence. Interestingly, the pathogenicity of these potentially reassortant strains was comparable to that of reference vvIBDV. All strains characterized in this study exhibited an antigenicity similar to the cognate reference IBDV strains. These data reveal the continuous genetic evolution of IBDV strains in Algerian poultry through reassortment and acquisition of genetic material of unidentified origin. Continuous surveillance of the situation as well as good vaccination practice associated with appropriate biosecurity measures are necessary for disease control.


Subject(s)
Birnaviridae Infections/virology , Infectious bursal disease virus/genetics , Infectious bursal disease virus/pathogenicity , Poultry Diseases/virology , Reassortant Viruses/genetics , Reassortant Viruses/pathogenicity , Algeria , Animals , Antibodies, Viral/immunology , Antigens, Viral/immunology , Birnaviridae Infections/immunology , Chickens/virology , Infectious bursal disease virus/classification , Infectious bursal disease virus/immunology , Molecular Epidemiology , Phylogeny , Poultry Diseases/immunology , Reassortant Viruses/classification , Reassortant Viruses/immunology
2.
Avian Pathol ; 47(2): 179-188, 2018 Apr.
Article in English | MEDLINE | ID: mdl-29039212

ABSTRACT

Infectious bursal disease virus (IBDV) is a Birnaviridae family member of economic importance for poultry. This virus infects and destroys developing B lymphocytes in the cloacal bursa, resulting in a potentially fatal or immunosuppressive disease in chickens. Naturally occurring viruses and many vaccine strains are not able to grow in in vitro systems without prior adaptation, which often affects viral properties such as virulence. Primary bursal cells, which are the main target cells of lymphotropic IBDV in vivo, may represent an attractive system for the study of IBDV. Unfortunately, bursal cells isolated from bursal follicles undergo apoptosis within hours following their isolation. Here, we demonstrate that ex vivo stimulation of bursal cells with phorbol 12-myristate 13-acetate maintains their viability long enough to allow IBDV replication to high titres. A wide range of field-derived or vaccine serotype 1 IBDV strains could be titrated in these phorbol 12-myristate 13-acetate -stimulated bursal cells and furthermore were permissive for replication of non-cell-culture-adapted viruses. These cells also supported multistep replication experiments and flow cytometry analysis of infection. Ex vivo-stimulated bursal cells therefore offer a promising tool in the study of IBDV.


Subject(s)
Bursa of Fabricius/cytology , Chickens , Infectious bursal disease virus/physiology , Virus Cultivation/veterinary , Animals , Cell Survival , Cells, Cultured , Tetradecanoylphorbol Acetate/pharmacology , Virus Cultivation/methods
3.
J Clin Endocrinol Metab ; 101(4): 1615-26, 2016 04.
Article in English | MEDLINE | ID: mdl-26829440

ABSTRACT

CONTEXT: Obesity alters adipose tissue's metabolic and endocrine functions and causes a chronic local and systemic low-grade inflammatory state to develop, generating obesity-associated complications. In the last decade, many entities contributing to and regulating this inflammatory state have been identified, among which are microRNAs. OBJECTIVE: This study aimed to identify microRNA regulated in inflamed adipocytes and adipose tissue, and its effect on adipocyte biology. DESIGN AND RESULTS: We screened the expression profile of TNFα-treated adipocytes (a major pro-inflammatory protein expressed in obese adipose tissue), and identified miR-155 as the most responsive microRNA. The involvement of TNFα on the basal miR-155 expression was confirmed in the adipose tissue of Tnfa−/− mice where miR-155 was significantly reduced. Also, mice overexpressing p65 or invalidated for p65 in adipose tissue respectively increased and decreased miR-155 expression, in line with the involvement of the nuclear factor κB (NF-κB) pathway in miR-155 induction. miR-155 expression was higher in obese subjects' adipose tissue than in that of normal-weight subjects, and correlated with TNFα expression and body mass index. Gain and loss of function of miR-155 showed its effect on adipocyte function, probably via its ability to target PPARγ mRNA 3'UTR. Interestingly, miR-155 overexpression also resulted in an increased inflammatory state in adipocytes. CONCLUSION: Altogether, these data are evidence of a proinflammatory loop mediated by NF-κB and miR-155 that could participate in the amplification of inflammatory status in adipocytes.


Subject(s)
Adipocytes/pathology , Adipose Tissue/pathology , Inflammation/etiology , MicroRNAs/genetics , Obesity/complications , Adipocytes/metabolism , Adipose Tissue/metabolism , Adult , Animals , Cells, Cultured , Humans , Inflammation/pathology , Male , Mice , Mice, Inbred C57BL , Mice, Knockout , Signal Transduction
SELECTION OF CITATIONS
SEARCH DETAIL
...