39 research outputs found
GaHV-2 ICP22 protein is expressed from a bicistronic transcript regulated by three GaHV-2 microRNAs
International audienceHerpesviruses have a lifecycle consisting of successive lytic, latent and reactivation phases. Only three infected cell proteins (ICPs) have been described for the oncogenic Marek's disease virus (or Gallid herpes virus 2, GaHV-2): ICP4, ICP22 and ICP27. We focus here on ICP22, confirming its cytoplasmic location and showing that ICP22 is expressed during productive phases of the lifecycle, via a bicistronic transcript encompassing the US10 gene. We also identified the unique promoter controlling ICP22 expression, and its core promoter, containing functional responsive elements including E-box, ETS-1 and GATA elements involved in ICP22 transactivation. ICP22 gene expression was weakly regulated by DNA methylation and activated by ICP4 or ICP27 proteins. We also investigated the function of GaHV-2 ICP22. We found that this protein repressed transcription from its own promoter and from those of IE ICP4 and ICP27, and the late gK promoter. Finally, we investigated posttranscriptional ICP22 regulation by GaHV-2 microRNAs. We found that mdv1-miR-M5-3p and -M1-5p downregulated ICP22 mRNA expression during latency, whereas, unexpectedly, mdv1-miR-M4-5p upregulated the expression of the protein ICP22, indicating a tight regulation of ICP22 expression by microRNAs
Heterogeneity of Persistence of Salmonella enterica Serotype Senftenberg Strains Could Explain the Emergence of this Serotype in Poultry Flocks
Salmonella enterica serotype Senftenberg (S. Senftenberg) has recently become more frequent in poultry flocks. Moreover some strains have been implicated in severe clinical cases. To explain the causes of this emergence in farm animals, 134 S. Senftenberg isolates from hatcheries, poultry farms and human clinical cases were analyzed. Persistent and non-persistent strains were identified in chicks. The non-persistent strains disappeared from ceca a few weeks post inoculation. This lack of persistence could be related to the disappearance of this serotype from poultry farms in the past. In contrast, persistent S. Senftenberg strains induced an intestinal asymptomatic carrier state in chicks similar to S. Enteritidis, but a weaker systemic infection than S. Enteritidis in chicks and mice. An in vitro analysis showed that the low infectivity of S. Senftenberg is in part related to its low capacity to invade enterocytes and thus to translocate the intestinal barrier. The higher capacity of persistent than non-persistent strains to colonize and persist in the ceca of chickens could explain the increased persistence of S. Senftenberg in poultry flocks. This trait might thus present a human health risk as these bacteria could be present in animals before slaughter and during food processing
Rift Valley Fever â epidemiological update and risk of introduction into Europe
Rift Valley fever (RVF) is a vector-borne disease transmitted by a broad spectrum of mosquito species, especially Aedes and Culex genus, to animals (domestic and wild ruminants and camels) and humans. Rift Valley fever is endemic in sub-Saharan Africa and in the Arabian Peninsula, with periodic epidemics characterised by 5â15 years of inter-epizootic periods. In the last two decades, RVF was notiïŹed in new African regions (e.g. Sahel), RVF epidemics occurred more frequently and low-level enzootic virus circulation has been demonstrated in livestock in various areas. Recent outbreaks in a French overseas department and some seropositive cases detected in Turkey, Tunisia and Libya raised the attention of the EU for a possible incursion into neighbouring countries. The movement of live animals is the most important pathway for RVF spread from the African endemic areas to North Africa and the Middle East. The movement of infected animals and infected vectors when shipped by ïŹights, containers or road transport is considered as other plausible pathways of introduction into Europe. The overall risk of introduction of RVF into EU through the movement of infected animals is very low in all the EU regions and in all MSs (less than one epidemic every 500 years), given the strict EU animal import policy. The same level of risk of introduction in all the EU regions was estimated also considering the movement of infected vectors, with the highest level for Belgium, Greece, Malta, the Netherlands (one epidemic every 228â700 years), mainly linked to the number of connections by air and sea transports with African RVF infected countries. Although the EU territory does not seem to be directly exposed to an imminent risk of RVFV introduction, the risk of further spread into countries neighbouring the EU and the risks of possible introduction of infected vectors, suggest that EU authorities need to strengthen their surveillance and response capacities, as well as the collaboration with North African and Middle Eastern countries.info:eu-repo/semantics/publishedVersio
Analysis of salmonella Senftenberg emergence in poultry production
En production avicole, S. Senftenberg connue pour ĂȘtre souvent associĂ©e au couvoir, est devenue trĂšs frĂ©quente dans les Ă©levages de volaille. Lâobjectif de la thĂšse est donc de comprendre les causes de cette persistance. Les rĂ©sultats prĂ©sentĂ©s suggĂšrent que lâexistence de souches persistantes au sein du sĂ©rovar Senftenberg peut ĂȘtre Ă lâorigine de lâaugmentation de sa prĂ©valence dans les Ă©levages. Nous avons en effet identifiĂ© des souches prĂ©sentant des phĂ©notypes distincts en termes de persistance dans les caeca de poulets. Les souches persistantes ont la capacitĂ© dâinduire un portage intestinal similaire Ă S. Enteritidis.Toutefois, les rĂ©sultats in vivo ont montrĂ© quâĂ la diffĂ©rence de S. Enteritidis, les souches de S.Senftenberg sont incapables dâinduire une forte infection systĂ©mique chez le poulet et la souris,probablement due Ă leur faible capacitĂ© Ă rĂ©sister aux cellules immunitaires. La comparaison entre les souches persistantes et non-persistantes nâa montrĂ© aucune diffĂ©rence de survie dans le contenu et le mucus caecal. Cependant, les souches persistantes ont une meilleure capacitĂ© Ă coloniser et persister dans les tissus dâanimaux ce qui pourrait ĂȘtre une explication possible Ă lâaugmentation de leur persistance. Ce caractĂšre pourrait donc prĂ©senter un risque pour la santĂ© humaine Ă©tant donnĂ© que ces bactĂ©ries peuvent ĂȘtre prĂ©sentes chez les animaux avant l'abattage et la transformation des aliments.In poultry production, S. Senftenberg was associated to the hatchery, but has recently become morefrequent in poultry farms. The aim of our study is to explain the increased persistence of this serovar. Our findings suggest that the existence of persistent strains within the serovar Senftenberg could explain its recent emergence in poultry flocks. We identified strains showing different persistence phenotypes inchicken caeca. The persistent strains are able to induce an intestinal asymptomatic carrier state in chicks similar to S. Enteritidis. However, the in vivo analysis showed that S. Senftenberg strains, contrary to S.Enteritidis are unable to induce a strong systemic infection in infected mice and chickens which could be in part related to their low capacity to resist to immune cells. The comparison between persistent and nonpersistents trains showed no difference in their ability to grow in the caecal content and mucus. However,persistent strains are more able to colonize and persist in chickens and mice tissues, which could be a possible explanation for their increased persistence. This trait might thus present a human health risk as these bacteria could be present in animals before slaughter and during food processing
Transcriptional and post-trancriptional regulation of the US1 gene encoding the Marek's disease virus ICP22 protein
Le virus de la maladie de Marek (GaHV-2), est un α-herpĂšsvirus induisant des lymphomes T chez le poulet. LâĂ©tude de la protĂ©ine IE ICP22 a montrĂ© que cette protĂ©ine est principalement asssociĂ©e Ă la phase lytique du cycle viral avec une localisation majoritairement cytoplasmique. Nos rĂ©sultats montrent que cette protĂ©ine rĂ©prime la transcription des promoteurs viraux. Par ailleurs, nous avons montrĂ© que la protĂ©ine Ă©tait produite Ă la fois Ă partir de deux transcrit, un transcrit monocistronique et un transcrit bicistronique de façon majoritaire. La transcription dâICP22 est pilotĂ©e par un promoteur unique dont nous avons localisĂ© le « core » promoteur dans les 200 nt en amont du gĂšne. Dans notre Ă©tude, nous avons montrĂ© que le promoteur du gĂšne ICP22 Ă©tait faiblement soumis au mĂ©canisme de mĂ©thylation. Ce promoteur peut ĂȘtre rĂ©gulĂ© par la protĂ©ine virale ICP4 connue pour ĂȘtre un transactivateur majeur au sein des alphaherpĂšsvirus. Enfin, nous avons mis en Ă©vidence quâICP22 Ă©tait la cible de 3 miR viraux parmi lesquels la cible prĂ©dite pour le mdv1-miR-M1 et mdv1-miR-M5-3p entraĂźnaient une diminution du taux du transcrit.Marekâs disease virus (GaHV-2) is an α-herpesvirus that induces T-cell lymphoma in chickens. The study of the IE ICP22 protein showed that this protein is mainly associated to the lytic phase of the viral cycle viral with a cytoplasmic localization. Our results showed that this protein represses the transcription of the viral promoters. ICP22 protein is produced from two transcript, a monocistronic and a bicistronic. The transcription of ICP22 is drived by a unique promoter whose "core" promoter was located in the 200 nt upstream to the gene. In our study, we showed that ICP22 promoter was weakly subjected to rĂ©gulation by methylation. This promoter is regulated by the viral protein ICP4 known to be a major transactivateur within alphaherpĂšsvirus. Finally, we highlighted that ICP22 was the target of 3 miR viral among which the target predicted for mdv1-miR-M1 and mdv1-miR-M5-3p decreased the rate of the ICP22 transcripts
Analyse de l'Ă©mergence de <em>Salmonella</em> Senftenberg dans les productions avicoles
En production avicole, S. Senftenberg connue pour ĂȘtre souvent associĂ©e au couvoir, est devenue trĂšs frĂ©quente dans les Ă©levages de volaille. L'objectif de la thĂšse est donc de comprendre les causes de cette persistance. Les rĂ©sultats prĂ©sentĂ©s suggĂšrent que l'existence de souches persistantes au sein du serovar Senftenberg peut ĂȘtre Ă l'origine de l'augmentation de sa prĂ©valence dans les Ă©levages. Nous avons en effet identifiĂ© des souches prĂ©sentant des phĂ©notypes distincts en termes de persistance dans les caeca de poulets. Les souches persistantes ont la capacitĂ© d'induire un portage intestinal similaire Ă S. Enteritidis. Toutefois, les rĂ©sultats in vivo ont montre quâĂ la diffĂ©rence de S. Enteritidis, les souches de S. Senftenberg sont incapables d'induire une forte infection systĂ©mique chez le poulet et la souris, probablement due a leur faible capacitĂ© a rĂ©sister aux cellules immunitaires. La comparaison entre les souches persistantes et non-persistantes n'a montre aucune diffĂ©rence de survie dans le contenu et le mucus caecal. Cependant, les souches persistantes ont une meilleure capacitĂ© a coloniser et persister dans les tissus d'animaux ce qui pourrait ĂȘtre une explication possible a l'augmentation de leur persistance. Ce caractĂšre pourrait donc prĂ©senter un risque pour la sante humaine Ă©tant donnĂ© que ces bactĂ©ries peuvent ĂȘtre prĂ©sentes chez les animaux avant l'abattage et la transformation des aliments
Multiple invasion mechanisms and different intracellular Behaviors: a new vision of Salmonella-host cell interaction
International audienceSalmonella is a facultative intracellular bacterium found within a variety of phagocytic and nonphagocytic cells in vitro and in vivo. For decades, it has been accepted that Salmonella can enter cells only through a Trigger mechanism mediated by a type three secretion system, called T3SS-1. However, recent researches have shown that this bacterium can use other invasion pathways mediating either Trigger or Zipper entry processes. Following eukaryotic cell invasion, Salmonella has to ensure its survival and proliferation within host cells. To do so, this bacterium resides either within a membrane-bound vacuole or freely within host cell cytosol. It is not clear why Salmonella has developed these alternate mechanisms for cell invasion and proliferation, but this provides a new insight into the mechanisms leading to Salmonella-induced diseases. Thus, the aim of this review is to show the evolution of Salmonella-host cell interaction paradigms by summarizing the different strategies used by Salmonella serotypes to invade and proliferate into eukaryotic cells