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.
Project description:Differential expression was determined in Calu-3 cells between mock infected and infected with H1N1 influenza virus A/Netherlands/602/2009 at nine time points post-infection. As a comparison, cells were also infected with A/CA/04/2009 H1N1 influenza virus at 4 time points post-infection.
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.
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.
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
Project description:To further understand the molecular pathogenesis of the 2009 pandemic H1N1 influenza virus infection, we profiled cellular miRNAs of lung tissue from BALB/c mice infected with influenza virus BJ501 and a mouse-adapted influenza virus A/Puerto Rico/8/34 (H1N1)(PR8) as a comparison.
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.
