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Bruce H Janke - One of the best experts on this subject based on the ideXlab platform.
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efficacy of inactivated Swine Influenza Virus vaccines against the 2009 a h1n1 Influenza Virus in pigs
Vaccine, 2010Co-Authors: Amy L Vincent, Bruce H Janke, Eraldo L Zanella, Janice R Ciaccizanella, Marcus E Kehrli, Alessio Lorusso, P C Gauger, Kelly M LagerAbstract:The gene constellation of the 2009 pandemic A/H1N1 Virus is a unique combination from Swine Influenza A Viruses (SIV) of North American and Eurasian lineages, but prior to April 2009 had never before been identified in Swine or other species. Although its hemagglutinin gene is related to North American H1 SIV, it is unknown if vaccines currently used in U.S. Swine would cross-protect against infection with the pandemic A/H1N1. The objective of this study was to evaluate the efficacy of inactivated vaccines prepared with North American Swine Influenza Viruses as well as an experimental homologous A/H1N1 vaccine to prevent infection and disease from 2009 pandemic A/H1N1. All vaccines tested provided partial protection ranging from reduction of pneumonia lesions to significant reduction in Virus replication in the lung and nose. The multivalent vaccines demonstrated partial protection; however, none was able to prevent all nasal shedding or clinical disease. An experimental homologous 2009 A/H1N1 monovalent vaccine provided optimal protection with no Virus detected from nose or lung at any time point in addition to amelioration of clinical disease. Based on cross-protection demonstrated with the vaccines evaluated in this study, the U.S. Swine herd likely has significant immunity to the 2009 A/H1N1 from prior vaccination or natural exposure. However, consideration should be given for development of monovalent homologous vaccines to best protect the Swine population thus limiting shedding and the potential transmission of 2009 A/H1N1 from pigs to people.
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experimental inoculation of pigs with pandemic h1n1 2009 Virus and hi cross reactivity with contemporary Swine Influenza Virus antisera
Influenza and Other Respiratory Viruses, 2010Co-Authors: Amy L Vincent, Kelly M Lager, Kay S Faaberg, Michelle Harland, Eraldo L Zanella, Janice R Ciaccizanella, Marcus E Kehrli, Bruce H JankeAbstract:Please cite this paper as: Vincent et al. (2010) Experimental inoculation of pigs with pandemic H1N1 2009 Virus and HI cross-reactivity with contemporary Swine Influenza Virus antisera. Influenza and Other Respiratory Viruses 4(2), 53–60 Background A novel A/H1N1 was identified in the human population in North America in April 2009. The gene constellation of the Virus was a combination from Swine Influenza A Viruses (SIV) of North American and Eurasian lineages that had never before been identified in Swine or other species. Objectives The objectives were to (i) evaluate the clinical response of Swine following experimental inoculation with pandemic H1N1 2009; (ii) assess serologic cross-reactivity between H1N1 2009 and contemporary SIV antisera; and (iii) develop a molecular assay to differentiate North American-lineage SIV from H1N1 2009. Methods Experiment 1: Weaned pigs were experimentally infected with A/California/04/2009 (H1N1). Experiment 2: The cross-reactivity of a panel of US SIV H1N1 or H1N2 antisera with three isolates of pandemic A/H1N1 was evaluated. Experiment 3: A polymerase chain reaction (PCR)-based diagnostic test was developed and validated on samples from experimentally infected pigs. Results and Conclusions In experiment 1, all inoculated pigs demonstrated clinical signs and lesions similar to those induced by endemic SIV. Viable Virus and antigen were only detected in the respiratory tract. In experiment 2, serologic cross-reactivity was limited against H1N1 2009 isolates, notably among Virus antisera from the same HA phylogenetic cluster. The limited cross-reactivity suggests North American pigs may not be fully protected against H1N1 2009 from previous exposure or vaccination and novel tests are needed to rapidly diagnose the introduction of H1N1 2009. In experiment 3, an RT–PCR test that discriminates between H1N1 2009 and endemic North American SIV was developed and validated on clinical samples.
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characterization of a newly emerged genetic cluster of h1n1 and h1n2 Swine Influenza Virus in the united states
Virus Genes, 2009Co-Authors: Amy L Vincent, Marie Gramer, Kelly M Lager, Juergen A Richt, Bruce H JankeAbstract:H1 Influenza A Viruses that were distinct from the classical Swine H1 lineage were identified in pigs in Canada in 2003–2004; antigenic and genetic characterization identified the hemagglutinin (HA) as human H1 lineage. The Viruses identified in Canadian pigs were human lineage in entirety or double (human–Swine) reassortants. Here, we report the whole genome sequence analysis of four human-like H1 Viruses isolated from U.S. Swine in 2005 and 2007. All four isolates were characterized as triple reassortants with an internal gene constellation similar to contemporary U.S. Swine Influenza Virus (SIV), with HA and neuraminidase (NA) most similar to human Influenza Virus lineages. A 2007 human-like H1N1 was evaluated in a pathogenesis and transmission model and compared to a 2004 reassortant H1N1 SIV isolate with Swine lineage HA and NA. The 2007 isolate induced disease typical of Influenza Virus and was transmitted to contact pigs; however, the kinetics and magnitude differed from the 2004 H1N1 SIV. This study indicates that the human-like H1 SIV can efficiently replicate and transmit in the Swine host and now co-circulates with contemporary SIVs as a distinct genetic cluster of H1 SIV.
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naturally occurring Influenza infection in a ferret mustela putorius furo colony
Journal of Veterinary Diagnostic Investigation, 2009Co-Authors: Abby R Patterson, Kyoungjin Yoon, Vickie L Cooper, Bruce H Janke, Phillip C GaugerAbstract:Tissue samples from 2 juvenile ferrets (Mustela putorius furo) from a colony that was undergoing an outbreak of respiratory disease were submitted to the Iowa State University Veterinary Diagnostic Laboratory. Microscopic examination of lung samples revealed bronchointerstitial pneumonia with necrotizing bronchiolitis. Influenza A Virus was detected in sections of formalin-fixed lung by immunohistochemistry and reverse transcription polymerase chain reaction assay. A field investigation of the premises and analysis of additional samples led to the confirmation and characterization of an Influenza Virus with high homology to contemporary reassortant H1N1 Swine Influenza Viruses. Although ferrets have been used extensively to research the virulence and transmissibility of avian, human, and Swine Influenza Virus strains, no published information exists on naturally occurring outbreaks of Swine Influenza in ferrets.
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Swine Influenza Virus zoonotic potential and vaccination strategies for the control of avian and Swine Influenzas
The Journal of Infectious Diseases, 2008Co-Authors: Eileen L Thacker, Bruce H JankeAbstract:Influenza Viruses are able to infect humans, Swine, and avian species, and Swine have long been considered a potential source of new Influenza Viruses that can infect humans. Swine have receptors to which both avian and mammalian Influenza Viruses bind, which increases the potential for Viruses to exchange genetic sequences and produce new reassortant Viruses in Swine. A number of genetically diverse Viruses are circulating in Swine herds throughout the world and are a major cause of concern to the Swine industry. Control of Swine Influenza is primarily through the vaccination of sows, to protect young pigs through maternally derived antibodies. However, Influenza Viruses continue to circulate in pigs after the decay of maternal antibodies, providing a continuing source of Virus on a herd basis. Measures to control avian Influenza in commercial poultry operations are dictated by the virulence of the Virus. Detection of a highly pathogenic avian Influenza (HPAI) Virus results in immediate elimination of the flock. Low-pathogenic avian Influenza Viruses are controlled through vaccination, which is done primarily in turkey flocks. Maintenance of the current HPAI Virus-free status of poultry in the United States is through constant surveillance of poultry flocks. Although current Influenza vaccines for poultry and Swine are inactivated and adjuvanted, ongoing research into the development of newer vaccines, such as DNA, live-Virus, or vectored vaccines, is being done. Control of Influenza Virus infection in poultry and Swine is critical to the reduction of potential cross-species adaptation and spread of Influenza Viruses, which will minimize the risk of animals being the source of the next pandemic.
Kelly M Lager - One of the best experts on this subject based on the ideXlab platform.
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efficacy of inactivated Swine Influenza Virus vaccines against the 2009 a h1n1 Influenza Virus in pigs
Vaccine, 2010Co-Authors: Amy L Vincent, Bruce H Janke, Eraldo L Zanella, Janice R Ciaccizanella, Marcus E Kehrli, Alessio Lorusso, P C Gauger, Kelly M LagerAbstract:The gene constellation of the 2009 pandemic A/H1N1 Virus is a unique combination from Swine Influenza A Viruses (SIV) of North American and Eurasian lineages, but prior to April 2009 had never before been identified in Swine or other species. Although its hemagglutinin gene is related to North American H1 SIV, it is unknown if vaccines currently used in U.S. Swine would cross-protect against infection with the pandemic A/H1N1. The objective of this study was to evaluate the efficacy of inactivated vaccines prepared with North American Swine Influenza Viruses as well as an experimental homologous A/H1N1 vaccine to prevent infection and disease from 2009 pandemic A/H1N1. All vaccines tested provided partial protection ranging from reduction of pneumonia lesions to significant reduction in Virus replication in the lung and nose. The multivalent vaccines demonstrated partial protection; however, none was able to prevent all nasal shedding or clinical disease. An experimental homologous 2009 A/H1N1 monovalent vaccine provided optimal protection with no Virus detected from nose or lung at any time point in addition to amelioration of clinical disease. Based on cross-protection demonstrated with the vaccines evaluated in this study, the U.S. Swine herd likely has significant immunity to the 2009 A/H1N1 from prior vaccination or natural exposure. However, consideration should be given for development of monovalent homologous vaccines to best protect the Swine population thus limiting shedding and the potential transmission of 2009 A/H1N1 from pigs to people.
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experimental inoculation of pigs with pandemic h1n1 2009 Virus and hi cross reactivity with contemporary Swine Influenza Virus antisera
Influenza and Other Respiratory Viruses, 2010Co-Authors: Amy L Vincent, Kelly M Lager, Kay S Faaberg, Michelle Harland, Eraldo L Zanella, Janice R Ciaccizanella, Marcus E Kehrli, Bruce H JankeAbstract:Please cite this paper as: Vincent et al. (2010) Experimental inoculation of pigs with pandemic H1N1 2009 Virus and HI cross-reactivity with contemporary Swine Influenza Virus antisera. Influenza and Other Respiratory Viruses 4(2), 53–60 Background A novel A/H1N1 was identified in the human population in North America in April 2009. The gene constellation of the Virus was a combination from Swine Influenza A Viruses (SIV) of North American and Eurasian lineages that had never before been identified in Swine or other species. Objectives The objectives were to (i) evaluate the clinical response of Swine following experimental inoculation with pandemic H1N1 2009; (ii) assess serologic cross-reactivity between H1N1 2009 and contemporary SIV antisera; and (iii) develop a molecular assay to differentiate North American-lineage SIV from H1N1 2009. Methods Experiment 1: Weaned pigs were experimentally infected with A/California/04/2009 (H1N1). Experiment 2: The cross-reactivity of a panel of US SIV H1N1 or H1N2 antisera with three isolates of pandemic A/H1N1 was evaluated. Experiment 3: A polymerase chain reaction (PCR)-based diagnostic test was developed and validated on samples from experimentally infected pigs. Results and Conclusions In experiment 1, all inoculated pigs demonstrated clinical signs and lesions similar to those induced by endemic SIV. Viable Virus and antigen were only detected in the respiratory tract. In experiment 2, serologic cross-reactivity was limited against H1N1 2009 isolates, notably among Virus antisera from the same HA phylogenetic cluster. The limited cross-reactivity suggests North American pigs may not be fully protected against H1N1 2009 from previous exposure or vaccination and novel tests are needed to rapidly diagnose the introduction of H1N1 2009. In experiment 3, an RT–PCR test that discriminates between H1N1 2009 and endemic North American SIV was developed and validated on clinical samples.
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characterization of a newly emerged genetic cluster of h1n1 and h1n2 Swine Influenza Virus in the united states
Virus Genes, 2009Co-Authors: Amy L Vincent, Marie Gramer, Kelly M Lager, Juergen A Richt, Bruce H JankeAbstract:H1 Influenza A Viruses that were distinct from the classical Swine H1 lineage were identified in pigs in Canada in 2003–2004; antigenic and genetic characterization identified the hemagglutinin (HA) as human H1 lineage. The Viruses identified in Canadian pigs were human lineage in entirety or double (human–Swine) reassortants. Here, we report the whole genome sequence analysis of four human-like H1 Viruses isolated from U.S. Swine in 2005 and 2007. All four isolates were characterized as triple reassortants with an internal gene constellation similar to contemporary U.S. Swine Influenza Virus (SIV), with HA and neuraminidase (NA) most similar to human Influenza Virus lineages. A 2007 human-like H1N1 was evaluated in a pathogenesis and transmission model and compared to a 2004 reassortant H1N1 SIV isolate with Swine lineage HA and NA. The 2007 isolate induced disease typical of Influenza Virus and was transmitted to contact pigs; however, the kinetics and magnitude differed from the 2004 H1N1 SIV. This study indicates that the human-like H1 SIV can efficiently replicate and transmit in the Swine host and now co-circulates with contemporary SIVs as a distinct genetic cluster of H1 SIV.
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failure of protection and enhanced pneumonia with a us h1n2 Swine Influenza Virus in pigs vaccinated with an inactivated classical Swine h1n1 vaccine
Veterinary Microbiology, 2008Co-Authors: Amy L Vincent, Bruce H Janke, Kelly M Lager, Marie R Gramer, Juergen A RichtAbstract:Two US Swine Influenza Virus (SIV) isolates, A/Swine/Iowa/15/1930 H1N1 (IA30) and A/Swine/Minnesota/00194/2003 H1N2 (MN03), were evaluated in an in vivo vaccination and challenge model. Inactivated vaccines were prepared from each isolate and used to immunize conventional pigs, followed by challenge with homologous or heterologous Virus. Both inactivated vaccines provided complete protection against homologous challenge. However, the IA30 vaccine failed to protect against the heterologous MN03 challenge. Three of the nine pigs in this group had substantially greater percentages of lung lesions, suggesting the vaccine potentiated the pneumonia. In contrast, priming with live IA30 Virus provided protection from nasal shedding and Virus replication in the lung in MN03 challenged pigs. These data indicate that divergent Viruses that did not cross-react serologically did not provide complete cross-protection when used in inactivated vaccines against heterologous challenge and may have enhanced disease. In addition, live Virus infection conferred protection against heterologous challenge.
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efficacy of intranasal administration of a truncated ns1 modified live Influenza Virus vaccine in Swine
Vaccine, 2007Co-Authors: Amy L Vincent, Adolfo Garciasastre, Bruce H Janke, Kelly M Lager, Richard J Webby, Jurgen A RichtAbstract:In the U.S., despite available Swine Influenza Virus (SIV) vaccines, multiple Influenza subtypes as well as antigenic and genetic variants within subtypes continue to circulate in the Swine population. One of the challenges to control and eliminate SIV is that the currently used inactivated Influenza Virus vaccines do not provide adequate cross-protection against multiple antigenic variants of SIV in the field. We previously generated a recombinant H3N2 Swine Influenza Virus (SIV) based on the Influenza A/SW/TX/4199-2/98 Virus (TX98) containing an NS1 gene expressing a truncated NS1 protein of 126 amino acids, TX98-NS1Δ126 Virus. This recombinant strain was demonstrated to be highly attenuated in Swine and showed potential for use as a modified live-Virus vaccine (MLV) after intratracheal application in pigs. However, this route of inoculation is not practical for vaccination in the field. In the present study, we first compared intramuscular and intranasal routes of application of the MLV, and found that the intranasal route was superior in priming the local (mucosal) immune response. Pigs were then vaccinated via the intranasal route and challenged with wild type homologous TX98 H3N2 Virus, with a genetic and antigenic variant H3N2 SIV (Influenza A/SW/CO/23619/99 Virus, CO99) and a heterosubtypic H1N1 SIV (Influenza A/SW/IA/00239/2004 Virus, IA04). The intranasally vaccinated pigs were completely protected against homologous challenge. In addition, MLV vaccination provided nearly complete protection against the antigenic H3N2 variant CO99 Virus. When challenged with the H1N1 IA04 Virus, MLV vaccinated animals displayed reduced fever and Virus titers despite minimal reduction in lung lesions. In vaccinated pigs, there was no serologic cross-reactivity by HI assays with the heterologous or heterosubtypic Viruses. However, there appeared to be substantial cross-reactivity in antibodies at the mucosal level with the CO99 Virus in MLV vaccinated pigs.
Zygmunt Pejsak - One of the best experts on this subject based on the ideXlab platform.
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coinfection modulates inflammatory responses clinical outcome and pathogen load of h1n1 Swine Influenza Virus and haemophilus parasuis infections in pigs
BMC Veterinary Research, 2017Co-Authors: Malgorzata Pomorskamol, Arkadiusz Dors, Krzysztof Kwit, Ewelina Czyzewskadors, Zygmunt PejsakAbstract:Respiratory co-infections are important factor affecting the profitability of pigs production. Swine Influenza Virus (SIV) may predispose to secondary infection. Haemophilus parasuis (Hps) can be a primary pathogen or be associated with other pathogens such as SIV. To date, little is known about the effect of coinfection with SIV and Hps on the disease severity and inflammatory response and the role of Hps in the induction of pneumonia in the absence of other respiratory pathogens. In the study we investigated the influence of SIV and Hps coinfection on clinical course, inflammatory response, pathogens shedding and load at various time points following intranasal inoculation. The correlation between local concentration of cytokines and severity of disease as well as serum acute phase proteins (APP) concentration has been also studied. All co-infected pigs had fever, while in single inoculated pigs fever was observed only in part of animals. Necropsy revealed lesions in the lungs all SIV-inoculated and co-inoculated pigs, while in Hps-single inoculated animals only 1 out of 11 pigs revealed gross lung lesions. The SIV shedding was the highest in co-inoculated pigs. There were no differences between Hps-single inoculated and co-inoculated groups with regard to Hps shedding. The significant increase in Hps titre in the lung has been found only in co-inoculated group. All APP increased after co-infection. In single-inoculated animals various kinetics of APP response has been observed. The lung concentrations of cytokines were induced mostly in SIV + Hps pigs in the apical and middle lobe. These results correlated well with localization of gross lung lesions. The results revealed that SIV increased the severity of lung lesions and facilitated Hps (PIWetHps192/2015) replication in the porcine lung. Furthermore, Hps influenced the SIV nasal shedding. Enhanced Hps and SIV replication, together with stronger systemic and local inflammatory response contributed to a more severe clinical signs and stronger, earlier immune response in co-inoculated animals. We confirmed the previous evidence that single-Hps infection does not produce significant pneumonic lesions but it should be in mind that other strains of Hps may produce lesions different from that reported in the present study.
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kinetics of single and dual infection of pigs with Swine Influenza Virus and actinobacillus pleuropneumoniae
Veterinary Microbiology, 2017Co-Authors: Malgorzata Pomorskamol, Arkadiusz Dors, Krzysztof Kwit, Andrzej Kowalczyk, Ewelina Stasiak, Zygmunt PejsakAbstract:Porcine respiratory disease complex (PRDC) is a common problem in modern pork production worldwide. Pathogens that are amongst other pathogens frequently involved in PRDC etiology are Swine Influenza Virus (SIV) and A. pleuropneumoniae. The effect of dual infection with mentioned pathogens has not been investigated to date. The aim of the present study was to evaluate the kinetics of single and dual infection of pigs with SIV and A. pleuropneumoniae with regard to clinical course, pathogens shedding, lung lesions and early immune response. The most severe symptoms were observed in co-inoculated piglets. The AUC value for SIV shedding was lower in pigs single inoculated with SIV as compared to co-inoculated animals. In contrast, no significant differences were found between A. pleuropneumoniae shedding in single or dual inoculated pigs. Three out of 5 co-inoculated piglets euthanized at 10 dpi were positive against serotype 2 A. pleuropneumonie. All piglets inoculated with SIV developed specific HI antibodies at 10 dpi. In pigs dual inoculated the specific humoral response against SIV was observed earlier, at 7 dpi. The SIV-like lung lesions were more severe in co-inoculated pigs. In the groups inoculated with A. pleuropneumoniae (single or dual) the acute phase protein response was generally stronger than in SIV-single infected group. Co-infection with SIV and A. pleuropneumoniae potentiated the severity of lung lesions caused by SIV and enhanced Virus replication in the lung and nasal SIV shedding. Enhanced SIV replication contributed to a more severe clinical course of the disease as well as earlier and higher magnitude immune response (acute phase proteins, HI antibodies) compared to single inoculated pigs.
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Coinfection modulates inflammatory responses, clinical outcome and pathogen load of H1N1 Swine Influenza Virus and Haemophilus parasuis infections in pigs
BMC, 2017Co-Authors: Małgorzata Pomorska-mól, Arkadiusz Dors, Krzysztof Kwit, Ewelina Czyżewska-dors, Zygmunt PejsakAbstract:Abstract Background Respiratory co-infections are important factor affecting the profitability of pigs production. Swine Influenza Virus (SIV) may predispose to secondary infection. Haemophilus parasuis (Hps) can be a primary pathogen or be associated with other pathogens such as SIV. To date, little is known about the effect of coinfection with SIV and Hps on the disease severity and inflammatory response and the role of Hps in the induction of pneumonia in the absence of other respiratory pathogens. In the study we investigated the influence of SIV and Hps coinfection on clinical course, inflammatory response, pathogens shedding and load at various time points following intranasal inoculation. The correlation between local concentration of cytokines and severity of disease as well as serum acute phase proteins (APP) concentration has been also studied. Results All co-infected pigs had fever, while in single inoculated pigs fever was observed only in part of animals. Necropsy revealed lesions in the lungs all SIV-inoculated and co-inoculated pigs, while in Hps-single inoculated animals only 1 out of 11 pigs revealed gross lung lesions. The SIV shedding was the highest in co-inoculated pigs. There were no differences between Hps-single inoculated and co-inoculated groups with regard to Hps shedding. The significant increase in Hps titre in the lung has been found only in co-inoculated group. All APP increased after co-infection. In single-inoculated animals various kinetics of APP response has been observed. The lung concentrations of cytokines were induced mostly in SIV + Hps pigs in the apical and middle lobe. These results correlated well with localization of gross lung lesions. Conclusions The results revealed that SIV increased the severity of lung lesions and facilitated Hps (PIWetHps192/2015) replication in the porcine lung. Furthermore, Hps influenced the SIV nasal shedding. Enhanced Hps and SIV replication, together with stronger systemic and local inflammatory response contributed to a more severe clinical signs and stronger, earlier immune response in co-inoculated animals. We confirmed the previous evidence that single-Hps infection does not produce significant pneumonic lesions but it should be in mind that other strains of Hps may produce lesions different from that reported in the present study
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profile of the porcine acute phase proteins response following experimental co infection with h3n2 Swine Influenza Virus and pasteurella multocida
Biomarkers, 2015Co-Authors: Malgorzata Pomorskamol, Krzysztof Kwit, K Stepniewska, I Markowskadaniel, Zygmunt PejsakAbstract:AbstractContext: Acute phase proteins (APPs) are proposed as potential markers of the health status in pigs.Objective: Circulating APPs in pigs co-infected with Swine Influenza Virus and Pasteurella multocida.Methods: Serum APPs were measured in co-infected and control pigs with the use of commercial ELISA tests.Results: All investigated APPs revealed significant changes in co-infected pigs during the study period. The concentration of C-reactive protein, haptoglobin and serum amyloid A (SAA) increased significantly at 2 dpi, before respiratory signs and fever were observed. Concentration of Pig-MAP increased significantly at 3 dpi. C-reactive protein and SAA reaction were rapid but short-lived. The concentration of Hp and Pig-MAP in serum also increased at very early stage of co-infection but remained elevated for a longer period of time.Conclusions: Maximal concentration of serum amyloid A correlated with the disease severity in pigs.
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c reactive protein haptoglobin serum amyloid a and pig major acute phase protein response in pigs simultaneously infected with h1n1 Swine Influenza Virus and pasteurella multocida
BMC Veterinary Research, 2013Co-Authors: Malgorzata Pomorskamol, Krzysztof Kwit, Iwona Markowskadaniel, K Stepniewska, Zygmunt PejsakAbstract:Background Swine Influenza (SI) is an acute respiratory disease caused by Swine Influenza Virus (SIV). Swine Influenza is generally characterized by acute onset of fever and respiratory symptoms. The most frequent complications of Influenza are secondary bacterial pneumonia. The objective of this work was to study the acute phase proteins (APP) responses after coinfection of piglets with H1N1 Swine Influenza Virus (SwH1N1) and Pasteurella multocida (Pm) in order to identify whether the individual APP response correlate with disease severity and whether APP could be used as markers of the health status of coinfected pigs.
Joaquim Segales - One of the best experts on this subject based on the ideXlab platform.
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Evaluation of the effectiveness of the SurePure Turbulator ultraviolet-C irradiation equipment on inactivation of different enveloped and non-enveloped Viruses inoculated in commercially collected liquid animal plasma
PloS one, 2019Co-Authors: Elena Blázquez, Joaquim Segales, Carmen Rodríguez, Jesús Ródenas, Nuria Navarro, Cristina Riquelme, Rosa Rosell, Joy M. Campbell, Joe D. Crenshaw, Joan PujolsAbstract:The objective of this study was to evaluate the effectiveness of the SurePure Turbulator ultraviolet-C (UV-C, 254 nm wavelength) irradiation equipment on inactivation of different enveloped and non-enveloped Viruses in commercially collected liquid animal plasma. Specifically, Pseudorabies Virus (PRV), Porcine reproductive and respiratory syndrome Virus (PRRSV), Porcine epidemic diarrhea Virus (PEDV), Bovine viral diarrhea Virus (BVDV), Classical Swine fever Virus (CSFV), Swine Influenza Virus (SIV) as enveloped Viruses and Porcine parvoVirus (PPV), Swine vesicular disease Virus (SVDV), Porcine circoVirus type 2 (PCV-2) and SenecaVirus A (SVA) as non-enveloped Viruses, were inoculated in bovine or porcine plasma and subjected to different UV-C irradiation doses (0, 750, 1500, 3000, 6000 and 9000 J/L) using an UV-C device developed for opaque liquid working under turbulent flow. The enveloped Viruses tested were inactivated at < 3000 J/L of UV-C, being the dose needed to inactivate 4 log TCID50 (4D) of 1612 J/L for PRV,1004 J/L for PRRSV, 1953 J/L for PEDV, 1639 J/L for SIV, 1641 J/L for CSFV and 1943 J/L for BVDV. The non-enveloped Viruses tended to have higher 4D values: 2161 J/L for PPV, 3223 J/L for SVA and 3708 J/L for SVDV. Because the initial viral concentration was
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Experimental infection with H1N1 European Swine Influenza Virus protects pigs from an infection with the 2009 pandemic H1N1 human Influenza Virus
Veterinary Research, 2010Co-Authors: Nuria Busquets, Joaquim Segales, Lorena Córdoba, Tufaria Mussá, Elisa Crisci, Gerard E. Martín-valls, Meritxell Simon-grifé, Marta Pérez-simó, Monica Pérez-maíllo, Jose I. NúñezAbstract:The recent pandemic caused by human Influenza Virus A(H1N1) 2009 contains ancestral gene segments from North American and Eurasian Swine lineages as well as from avian and human Influenza lineages. The emergence of this A(H1N1) 2009 poses a potential global threat for human health and the fact that it can infect other species, like pigs, favours a possible encounter with other Influenza Viruses circulating in Swine herds. In Europe, H1N1, H1N2 and H3N2 subtypes of Swine Influenza Virus currently have a high prevalence in commercial farms. To better assess the risk posed by the A(H1N1) 2009 in the actual situation of Swine farms, we sought to analyze whether a previous infection with a circulating European avian-like Swine A/Swine/Spain/53207/2004 (H1N1) Influenza Virus (hereafter referred to as SwH1N1) generated or not cross-protective immunity against a subsequent infection with the new human pandemic A/Catalonia/63/2009 (H1N1) Influenza Virus (hereafter referred to as pH1N1) 21 days apart. Pigs infected only with pH1N1 had mild to moderate pathological findings, consisting on broncho-interstitial pneumonia. However, pigs inoculated with SwH1N1 Virus and subsequently infected with pH1N1 had very mild lung lesions, apparently attributed to the remaining lesions caused by SwH1N1 infection. These later pigs also exhibited boosted levels of specific antibodies. Finally, animals firstly infected with SwH1N1 Virus and latter infected with pH1N1 exhibited undetectable viral RNA load in nasal swabs and lungs after challenge with pH1N1, indicating a cross-protective effect between both strains.
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detection of porcine reproductive and respiratory syndrome Virus porcine circoVirus type 2 Swine Influenza Virus and aujeszky s disease Virus in cases of porcine proliferative and necrotizing pneumonia pnp in spain
Veterinary Microbiology, 2007Co-Authors: Llorenc Grauroma, Joaquim SegalesAbstract:Proliferative and necrotizing pneumonia (PNP) is a severe form of interstitial pneumonia characterised by hypertrophy and proliferation of pneumocytes type 2 and presence of necrotic cells within alveoli lumen. Many viral agents have been linked to PNP aetiology, with especial emphasis on porcine reproductive and respiratory syndrome Virus (PRRSV). To gain knowledge on PNP causality, a retrospective study on 74 PNP cases from postweaning pigs from Spain was carried out. Coupled with histopathological examinations, the presence of porcine circoVirus type 2 (PCV2) by in situ hybridization (ISH), and PRRSV, Swine Influenza Virus (SIV) and Aujeszky's disease Virus (ADV) by immunohistochemical (IHC) methods, were investigated. PCV2 was the most prevalent viral agent in PNP cases (85.1%) followed by PRRSV (44.6%); 39.1% of PNP cases showed PCV2 as the solely detected agent, while only 4.1% had PRRSV as the unique pathogen. SIV and ADV were very sporadically detected in PNP cases, and always in co-infection with PCV2. Therefore, present data indicate that PCV2 is the most important aetiological agent in PNP cases from Spain and that PRRSV is not essential for the development of PNP. Taking into account the presented results and available literature, we suggest that PCV2 is possibly the main contributor to PNP cases in Europe while PRRSV could play a similar role in North America.
Peter Palese - One of the best experts on this subject based on the ideXlab platform.
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hemagglutinin stalk reactive antibodies are boosted following sequential infection with seasonal and pandemic h1n1 Influenza Virus in mice
Journal of Virology, 2012Co-Authors: Florian Krammer, Rong Hai, Natalie Pica, Gene S Tan, Peter PaleseAbstract:Previously, it has been shown that infection in humans with the pandemic Swine Influenza Virus induces antibodies with specificity to the stalk domain of the viral hemagglutinin. Following the generation of these data, we sought to recapitulate these findings in the mouse model by sequential Influenza Virus infection. Mice that were inoculated with a seasonal Influenza H1N1 Virus followed by infection with a pandemic H1N1 strain produced higher antihemagglutinin stalk antibody titers than mice sequentially infected with drifted seasonal strains. In order to achieve antibody titers of comparable magnitude using sequential infection, mice had to be infected with 100- to 1,000-fold more of the drifted seasonal Virus. The antistalk antibodies produced by these infections were Influenza Virus neutralizing, which illustrates the utility of the mouse model in which to study this interaction between Virus and host.
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the m segment of the 2009 new pandemic h1n1 Influenza Virus is critical for its high transmission efficiency in the guinea pig model
Journal of Virology, 2011Co-Authors: Yiying Chou, Anice C Lowen, Adolfo Garciasastre, Peter Palese, Randy A Albrecht, Natalie Pica, Jurgen A Richt, Rong HaiAbstract:A remarkable feature of the 2009 pandemic H1N1 Influenza Virus is its efficient transmissibility in humans compared to that of precursor strains from the triple-reassortant Swine Influenza Virus lineage, which cause only sporadic infections in humans. The viral components essential for this phenotype have not been fully elucidated. In this study, we aimed to determine the viral factors critical for aerosol transmission of the 2009 pandemic Virus. Single or multiple segment reassortments were made between the pandemic A/California/04/09 (H1N1) (Cal/09) Virus and another H1N1 strain, A/Puerto Rico/8/34 (H1N1) (PR8). These Viruses were then tested in the guinea pig model to understand which segment of Cal/09 Virus conferred transmissibility to the poorly transmissible PR8 Virus. We confirmed our findings by generating recombinant A/Swine/Texas/1998 (H3N2) (sw/Tx/98) Virus, a representative triple-reassortant Swine Virus, containing segments of the Cal/09 Virus. The data showed that the M segment of the Cal/09 Virus promoted aerosol transmissibility to recombinant Viruses with PR8 and sw/Tx/98 Virus backgrounds, suggesting that the M segment is a critical factor supporting the transmission of the 2009 pandemic Virus.
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unraveling the mystery of Swine Influenza Virus
Cell, 2009Co-Authors: Taia T Wang, Peter PaleseAbstract:Influenza Virus outbreaks occur with regularity, but the severity of outbreaks is not consistent. The recent flu epidemic caused by an H1N1 Swine Influenza Virus presents an opportunity to examine what is known about virulence factors and the spread of infection to better prepare for major Influenza outbreaks in the future.
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a novel Influenza a Virus mitochondrial protein that induces cell death
Nature Medicine, 2001Co-Authors: Weisan Chen, Paul A Calvo, Daniela Malide, James P Gibbs, Ulrich Schubert, Igor Bacik, Sameh Basta, Robert E Oneill, Jeanne Schickli, Peter PaleseAbstract:While searching for alternative reading-frame peptides encoded by Influenza A Virus that are recognized by CD8+ T cells, we found an abundant immunogenic peptide encoded by the +1 reading frame of PB1. This peptide derives from a novel conserved 87-residue protein, PB1-F2, which has several unusual features compared with other Influenza gene products in addition to its mode of translation. These include its absence from some animal (particularly Swine) Influenza Virus isolates, variable expression in individual infected cells, rapid proteasome-dependent degradation and mitochondrial localization. Exposure of cells to a synthetic version of PB1-F2 induces apoptosis, and Influenza Viruses with targeted mutations that interfere with PB1-F2 expression induce less extensive apoptosis in human monocytic cells than those with intact PB1-F2. We propose that PB1-F2 functions to kill host immune cells responding to Influenza Virus infection.
