Surveillance of Swine Influenza A Virus in Pigs
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PROVIDER: PRJEB97103 | ENA |
REPOSITORIES: ENA
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Project description:Swine H1N1 influenza virus and streptococcus suis serotype 2 (SS2) are two important contributors to the porcine respiratory disease complex, which have significant economic impacts. Clinically, swine influenza virus and swine streptococcus suis co-infection is common, which will increase the mortality. However, the pathogenesis of the co-infection remains largely unkown. To explore it, gene expression profiling was to performed to detect comprehensive analysis of the global host response induced by H1N1 virus infection alone, SS2 infection alone, H1N1-SS2 co-infection and PBS control.
2016-09-10 | GSE60172 | GEO
Project description:As a mild, highly contagious, respiratory disease, swine influenza always damages the innate immune systems, and increases susceptibility to secondary infections which results in considerable morbidity and mortality in pigs. Nevertheless, the systematical host response of pigs to swine influenza virus infection remains largely unknown. To explore these, a time-course gene expression profiling was performed to detect comprehensive analysis of the global host response induced by H1N1 swine influenza virus in pigs.
2011-04-27 | GSE28871 | GEO
Project description:As a mild, highly contagious, respiratory disease, swine influenza always damages the innate immune systems, and increases susceptibility to secondary infections which results in considerable morbidity and mortality in pigs. Nevertheless, the systematical host response of pigs to swine influenza virus infection remains largely unknown. To explore these, a time-course gene expression profiling was performed to detect comprehensive analysis of the global host response induced by H1N1 swine influenza virus in pigs. At the age of day 35, 15 pigs were randomly allocated to the non-infected group and 15 to the infected group. Each piglet of the infected group was intranasaly challenged with A/swine/Hubei/101/2009(H1N1) strain and Each piglet of the non-infected group was treated similarly with an identical volume of PBS as control.
2011-04-27 | E-GEOD-28871 | biostudies-arrayexpress
Project description:In order to identify the swine genes which play roles in the regulation of swine influenza A virus replication, the gene microarray was performed to explore the systematical host response to the swine H1N1/2009 influenza A virus infection in porcine cells.
2017-03-24 | GSE96952 | GEO
Project description:In recent years, the roles of microRNAs playing in the regulation of influenza viruses replication caused researchers' much attenion. However, much work focused on the interactions between human, mice or chicken microRNAs with human or avian influenza viruses rather than the interactions of swine microRNAs and swine influenza viruses. To investigate the roles of swine microRNAs playing in the regulation of swine influenza A virus replication, the microRNA microarray was performed to identify which swine microRNAs were involved in swine H1N1/2009 influenza A virus infection.
2017-03-24 | GSE96953 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE35738: 2009 pandemic H1N1 virus causes disease and upregulation of genes related to inflammatory and immune response, cell death, and lipid metabolism in pigs GSE40088: Comparative transcriptomic analysis of acute host responses during 2009 pandemic H1N1 influenza infection in mouse, macaque, and swine (macaque dataset) GSE40091: Comparative transcriptomic analysis of acute host responses during 2009 pandemic H1N1 influenza infection in mouse, macaque, and swine (mouse dataset) Refer to individual Series
2012-08-13 | E-GEOD-40092 | biostudies-arrayexpress
Project description:Purpose: The goals of this study is to analyze differentially expressed microRNAs in pulmonary alveolar macrophages from pigs infected with H1N1 swine influenza A virus at different time points. Methods: miRNA profiles in PAMs from pigs infected with H1N1 SwIV at three time points were generated by deep sequencing. Differentially expressed miRNAs were then identified and their targets were predicted. For these targets, GO and KEGG analyses were performed and protein-protein interaction networks regulated by DE miRNAs were constructed. Results: Comparing to control group, 70 and 16 DE miRNAs were respectively identified on post-infection day (PID) 4 and PID 7. 56 DE miRNAs were identified between PID4 and PID7. GO and KEGG analyses indicated that most of targets for these DE miRNAs were related to immune and inflammatory responses. Conclusions: Our study represents the first integrative analysis of DE miRNAs in PAMs infected with H1N1 SwIV at different time points. The results in this study would enable us to better understand the underlying pathogenesis of H1N1 SwIV infection in pigs. Furthermore, these data would be very useful for investigating the functions and regulatory mechanisms of miRNAs in human influenza because pig serves as an excellent animal model to study human diseases.
2014-07-17 | GSE49249 | GEO
Project description:Purpose: The goals of this study is to analyze differentially expressed microRNAs in pulmonary alveolar macrophages from pigs infected with H1N1 swine influenza A virus at different time points. Methods: miRNA profiles in PAMs from pigs infected with H1N1 SwIV at three time points were generated by deep sequencing. Differentially expressed miRNAs were then identified and their targets were predicted. For these targets, GO and KEGG analyses were performed and protein-protein interaction networks regulated by DE miRNAs were constructed. Results: Comparing to control group, 70 and 16 DE miRNAs were respectively identified on post-infection day (PID) 4 and PID 7. 56 DE miRNAs were identified between PID4 and PID7. GO and KEGG analyses indicated that most of targets for these DE miRNAs were related to immune and inflammatory responses. Conclusions: Our study represents the first integrative analysis of DE miRNAs in PAMs infected with H1N1 SwIV at different time points. The results in this study would enable us to better understand the underlying pathogenesis of H1N1 SwIV infection in pigs. Furthermore, these data would be very useful for investigating the functions and regulatory mechanisms of miRNAs in human inM-oM-,M-^Buenza because pig serves as an excellent animal model to study human diseases. miRNA profiles in PAMs from pigs infected with H1N1 SwIV at three time points were generated by deep sequencing.
2014-07-17 | E-GEOD-49249 | biostudies-arrayexpress
Project description:The determinants of influenza transmission remain poorly understood. Swine influenza viruses preferentially attach to receptors found in the upper airways; however, most swine influenza viruses fail to transmit efficiently from swine to humans, and from human-to-human. The pandemic 2009 H1N1 (H1N1pdm) virus was a rare exception of a swine virus that acquired efficient transmissibility from human-to-human, and is reflected in efficient respiratory droplet transmission in ferrets. We hypothesize that virus-induced host responses in the upper airways correlate with airborne transmission in ferrets. To address this question, we used the H1N1pdm virus and swine influenza A/swine/Hong Kong/201/2010 (HK201) virus that has comparable titre in the ferret nasopharynx, but it exhibits differential transmissibility in ferrets via respiratory droplet route. We performed a transcriptomic analysis of tissues from the upper and lower respiratory tract from ferrets infected with either H1N1pdm or HK201 viruses using ferret-specific Agilent oligonucleotide arrays. We found differences in the kinetics of the innate immune response elicited by these two viruses that varied across tissues.
2017-03-31 | GSE79282 | GEO
Project description:In June 2009, the World Health Organization declared the first influenza pandemic of the 21st century, due to the emergence and rapid spread of new swine origin H1N1 influenza A virus. In contrast to seasonal influenza infections, which typically cause morbidity and mortality in the elderly, this virus caused severe infection in young adults and not the elderly. This phenomenon was attributed to the presence of cross-neutralizing antibodies acquired by older individuals from previous exposure to swine origin influenza. However, this hypothesis could not be empirically tested using clinical data. To address this question, we investigated viral replication and the development of the immune response in naï12 years old) and aged (20 to 24 years old) female rhesus macaques infected with A/California/04/2009 (H1N1), one of the circulating pandemic strains in 2009. We compared viral loads as well as the kinetics and magnitude of the adaptive immune response in peripheral blood and bronchoalveolar lavage samples (BAL) collected longitudinally for 99 days post-infection. Although, adult animals exhibited earlier T cell responses in peripheral blood, aged animals generated a robust T cell response with comparable kinetics and magnitude as those observed in young animals in BAL. Moreover, aged animals generated a higher hemagglutination inhibition titer compared to young animals. We also measured the concentration of several cytokines in BAL supernatant. With the exception of IL-8, which was higher in aged animals, we found no differences in IFNa, IFNb, TNFa, IL-1r, IL-6, IL-15, IL-17, or MCP1 levels. Finally, we compared gene expression infection using microarray analysis of BAL samples taken on days 0, 4, 7, 10, and 14 pi. Our analyses revealed that the largest difference in host response between aged and young animals was detected day 4 post-infection, with significant enrichment for genes associated with inflammation, the innate immune response, and T cell activation in aged animals. The ability of aged animals to generate a robust immune response, especially antibody response, following infection with 2009 H1N1 virus could explain the lack of morbidity normally observed with seasonal influenza viruses in this vulnerable population.
2012-06-06 | GSE38502 | GEO