Emergence of a New Swine H3N2 and Pandemic (H1N1) 2009 Influenza A Virus Reassortant in Two Canadian Animal Populations, Mink and Swine

A swine H3N2 (swH3N2) and pandemic (H1N1) 2009 (pH1N1) influenza A virus reassortant (swH3N2/ pH1N1) was detected in Canadian swine at the end of 2010. Simultaneously, a similar virus was also detected in Canadian mink based on partial viral genome sequencing. The origin of the new swH3N2/pH1N1 viral genes was related to the North American swH3N2 triple-reassortant cluster IV (for hemagglutinin [HA] and neuraminidase [NA] genes) and to pH1N1 for all the other genes (M, NP, NS, PB1, PB2, and PA). Data indicate that the swH3N2/pH1N1 virus can be found in several pigs that are housed at different locations.

Characterization of a Canadian mink H3N2 influenza A virus isolate genetically related to triple reassortant swine influenza virus.

In 2007, an H3N2 influenza A virus was isolated from Canadian mink. This virus was found to be phylogenetically related to a triple reassortant influenza virus which emerged in Canadian swine in 2005, but it is antigenically distinct. The transmission of the virus from swine to mink seems to have occurred following the feeding of animals with a ration composed of uncooked meat by-products of swine obtained from slaughterhouse facilities. Serological analyses suggest that the mink influenza virus does not circulate in the swine population. Presently, the prevalence of influenza virus in Canadian farmed and wild mink populations is unknown. The natural occurrence of influenza virus infection in mink with the presence of clinical signs is a rare event that deserves to be reported.

Capsular sialic acid of Streptococcus suis serotype 2 binds to swine influenza virus and enhances bacterial interactions with virus-infected tracheal epithelial cells.

Streptococcus suis serotype 2 is an important swine bacterial pathogen, and it is also an emerging zoonotic agent. It is unknown how S. suis virulent strains, which are usually found in low quantities in pig tonsils, manage to cross the first host defense lines to initiate systemic disease. Influenza virus produces a contagious infection in pigs which is frequently complicated by bacterial coinfections, leading to significant economic impacts. In this study, the effect of a preceding swine influenza H1N1 virus (swH1N1) infection of swine tracheal epithelial cells (NTPr) on the ability of S. suis serotype 2 to adhere to, invade, and activate these cells was evaluated. Cells preinfected with swH1N1 showed bacterial adhesion and invasion levels that were increased more than 100-fold compared to those of normal cells. Inhibition studies confirmed that the capsular sialic acid moiety is responsible for the binding to virus-infected cell surfaces. Also, preincubation of S. suis with swH1N1 significantly increased bacterial adhesion to/invasion of epithelial cells, suggesting that S. suis also uses swH1N1 as a vehicle to invade epithelial cells when the two infections occur simultaneously. Influenza virus infection may facilitate the transient passage of S. suis at the respiratory tract to reach the bloodstream and cause bacteremia and septicemia. S. suis may also increase the local inflammation at the respiratory tract during influenza infection, as suggested by an exacerbated expression of proinflammatory mediators in coinfected cells. These results give new insight into the complex interactions between influenza virus and S. suis in a coinfection model.

Prevalence et caracterisation de Staphylococcus aureus resistant a la methicilline d'origine aviaire au Quebec

Le Staphylococcus aureus résistant à la méthicilline (SARM) est un enjeu majeur en santé publique. Il est responsable d’une grande variété d’infections. Les “Livestock Associated-MRSA” (LA-MRSA) sont des SARM ayant comme origine les animaux de production tels le porc ou la volaille. Ils constituent un risque de transmission à l’humain via la chaîne alimentaire. Les LA-MRSA peuvent former du biofilm ce qui augmente leur tolérance aux stress environnementaux. Le biofilm est partiellement régulé par le système Agr. Il n’existe aucune donnée sur les ‘LA-MRSA’ d’origine aviaire au Québec. Les objectifs de ce projet étaient : (i) de déterminer la prévalence de ces SARM dans la viande de poulet et le poulet à griller de la province de Québec et (ii) de caractériser les isolats retrouvés. La collecte d’échantillons s’est effectuée dans 43 épiceries (309 cuisses et pilons de poulet) et dans deux abattoirs (échantillons nasaux et fécaux de 200 poulets) de la Montérégie. La prévalence de SARM a été évaluée à 1.29% (IC 95%: 0.35-3.28) et 0% dans la viande et les oiseaux respectivement. Les isolats testés se sont révélés résistants aux bêta-lactamines (n=15), à la tétracycline (n=10), à l’oxytétracycline (n=10), à la spectinomycine (n=10) et à la tobramycine (n=1). Le typage a révélé deux clones différents (ST398-V, n=10; et ST8-IVa ’USA300’, n=5). La présence de gènes de résistance aux antibiotiques (blaZ, blaR, blaI, erm(A), lnu(A), aad(D), fosB, tet(K), tet(L) et spc) ainsi que plusieurs gènes codant pour l’évasion du système immunitaire (IEC), la production de toxines ou encore pour la production de biofilm ont aussi été détectés. Une forte production de biofilm a été observée pour la majorité des isolats (n=11) à l’exception de certains isolats ST398. Le taux d’expression du système Agr n’a révélé aucune différence particulière entre les SARM testés. Pour conclure, nos données indiquent une faible prévalence de SARM chez la volaille et la viande de poulet. Les isolats ont été catégorisés en deux génotypes, dont un portant plus de gènes de résistance aux antibiotiques (ST398) et l’autre possédant plus de gènes de virulence (ST8).

Caractérisation et évaluation de la virulence de souches cliniques de Clostridium perfringens chez le poulet à griller élevé sans antibiotique.

réalisé en cotutelle avec Marie Archambault

Modelling scenarios of diffusion and control of pandemic influenza, italy

En aquest article es resumeixen els resultats publicats en un informe de l' ISS (Istituto Superiore di Sanità) del desembre de 2006, sobre un model matemàtic desenvolupat per un grup de treball que inclou a investigadors de les Universitats de Trento, Pisa i Roma, i els Instituts Nacionals de Salut (Istituto Superiore di Sanità, ISS), per avaluar i mesurar l'impacte de la transmissió i el control de la pandèmia de grip

Evaluación del programa de vigilancia centinela de influenza y otros virus respiratorios 1997- 2007 Colombia

La influenza es una entidad clínica, que es causada por los virus de la influenza A, B y C del género Influenza. El virus de la influenza A se clasifica en subtipos, con base en 2 antígenos de superficie: la hemaglutinina y la neuraminidasa. La respuesta inmune frente a estos antígenos (especialmente frente a la hemaglutinina), disminuye la probabilidad de infección, así como la severidad del cuadro clínico. La intención de este trabajo es describir el funcionamiento del programa de vigilancia centinela de influenza y otros virus respiratorios en Colombia, que permite identificar en que medida se alcanza la finalidad de esta actividad y que dificultades en general afectan su funcionamiento.

Infecciones respiratorias agudas en menores de 5 años vacunados o no contra la Influenza en el periodo del 2004 y 2005

De las enfermedades posibles que afectan el ser humano, las infecciones respiratorias agudas (IRA) son las más prevalentes de todas, con una prevalencia para Colombia según informes de la OPS del año 2005 de 12.6% en niños de 0 a 4 años. A pesar de la naturaleza en su mayoría son de corta duración y su desarrollo es benigno, con lleva repercusiones importantes en la salud y en lo económico: Es una de las principales causas de demanda de servicios médicos, de prescripción injustificada de antibióticos , de ausentismo escolar y laboral secundario. El objetivo de este estudio es comparar el número de eventos de infecciones respiratorias agudas, en niños entre 2 y 5 años de edad afiliados a la EPS Sanitas que consultaron al Clinisanitas de Ciudad Salitre entre el periodo de septiembre del 2004 y febrero del 2006, para determinar si existe o no asociación al hecho de estar vacunado contra la influenza.

Mutations in H5N1 influenza virus hemagglutinin that confer binding to human tracheal airway epithelium

The emergence in 2009 of a swine-origin H1N1 influenza virus as the first pandemic of the 21st Century is a timely reminder of the international public health impact of influenza viruses, even those associated with mild disease. The widespread distribution of highly pathogenic H5N1 influenza virus in the avian population has spawned concern that it may give rise to a human influenza pandemic. The mortality rate associated with occasional human infection by H5N1 virus approximates 60%, suggesting that an H5N1 pandemic would be devastating to global health and economy. To date, the H5N1 virus has not acquired the propensity to transmit efficiently between humans. The reasons behind this are unclear, especially given the high mutation rate associated with influenza virus replication. Here we used a panel of recombinant H5 hemagglutinin (HA) variants to demonstrate the potential for H5 HA to bind human airway epithelium, the predominant target tissue for influenza virus infection and spread. While parental H5 HA exhibited limited binding to human tracheal epithelium, introduction of selected mutations converted the binding profile to that of a current human influenza strain HA. Strikingly, these amino-acid changes required multiple simultaneous mutations in the genomes of naturally occurring H5 isolates. Moreover, H5 HAs bearing intermediate sequences failed to bind airway tissues and likely represent mutations that are an evolutionary "dead end." We conclude that, although genetic changes that adapt H5 to human airways can be demonstrated, they may not readily arise during natural virus replication. This genetic barrier limits the likelihood that current H5 viruses will originate a human pandemic.

Probing the receptor interactions ofan H5 avian influenza virus using a baculovirus expression system and functionalised poly(acrylic acid) ligands

Influenza viruses attach to host cells by binding to terminal sialic acid (Neu5Ac) on glycoproteins or glycolipids. Both the linkage of Neu5Ac and the identity of other carbohydrates within the oligosaccharide are thought to play roles in restricting the host range of the virus. In this study, the receptor specificity of an H5 avian influenza virus haemagglutinin protein that has recently infected man (influenza strain A/Vietnam/1194/04) has been probed using carbohydrate functionalised poly(acrylic acid) polymers. A baculovirus expression system that allows facile and safe analysis of the Neu5Ac binding specificity of mutants of H5 HA engineered at sites that are predicted to effect a switch in host range has also been developed. (C) 2007 Elsevier Ltd. All rights reserved.

NS1 proteins of avian influenza A viruses can act as antagonists of the human alpha/beta interferon response

Many viruses, including human influenza A virus, have developed strategies for counteracting the host type I interferon (IFN) response. We have explored whether avian influenza viruses were less capable of combating the type I IFN response in mammalian cells, as this might be a determinant of host range restriction. A panel of avian influenza viruses isolated between 1927 and 1997 was assembled. The selected viruses showed variation in their ability to activate the expression of a reporter gene under the control of the IFN-beta promoter and in the levels of IFN induced in mammalian cells. Surprisingly, the avian NS1 proteins expressed alone or in the genetic background of a human influenza virus controlled IFN-beta induction in a manner similar to the NS1 protein of human strains. There was no direct correlation between the IFN-beta induction and replication of avian influenza viruses in human A549 cells. Nevertheless, human cells deficient in the type I IFN system showed enhanced replication of the avian viruses studied, implying that the human type I IFN response limits avian influenza viruses and can contribute to host range restriction.

Development of a reverse genetics system enabling the rescue of recombinant avian influenza virus A/Turkey/England/50-92/91 (H5N1)

We previously described the use of an established reverse genetics system for the generation of recombinant human influenza A viruses from cloned cDNAs. Here, we have assembled a set of plasmids to allow recovery of the avian H5N1 influenza virus A/Turkey/England/50-92/91 entirely from cDNA. This system enables us to introduce mutations or truncations into the cDNAs to create mutant viruses altered specifically in a chosen gene. These mutant viruses can then be used in future pathogenesis studies in chickens and in studies to understand the host range restrictions of avian influenza viruses in humans.