Project description:Our understanding of the synergism between S. pneumoniae and influenza virus remains incomplete. The classic dogma has been that influenza attenuates the host innate immunity and increase the susceptibility to subsequent bacterial infection. Therefore, the majority of current studies have been focusing on the interaction of S. pneumoniae and influenza in the context of host cells. By contrast, in this study, we set out to investigate the response of pneumococcus alone to virus infection. Our hypothesis was that prior to causing any damages to host cells, influenza may have induced (lethal) changes to pneumococcus cell itself. Indeed, a very recent evidence has shown that direct viral treatment to pneumococcus will increase its adhesion to macrophage cells. Here, using quantitative phosphoproteomic approach, we attempt to investigate the global alterations of S. pneumoniae phosphorylation by influenza virus challenge, and provide a landscape of synergism between the IAV and pneumococcus.
Project description:Our understanding of the synergism between S. pneumoniae and influenza virus remains incomplete. The classic dogma has been that influenza attenuates the host innate immunity and increase the susceptibility to subsequent bacterial infection. Therefore, the majority of current studies have been focusing on the interaction of S. pneumoniae and influenza in the context of host cells. By contrast, in this study, we set out to investigate the response of pneumococcus alone to virus infection. Our hypothesis was that prior to causing any damages to host cells, influenza may have induced (lethal) changes to pneumococcus cell itself. Indeed, a very recent evidence has shown that direct viral treatment to pneumococcus will increase its adhesion to macrophage cells. Here, using quantitative shotgun approach, we attempt to investigate the proteomic alterations of S. pneumoniae by influenza virus challenge, and provide a landscape of interactions between the IAV and pneumococcus.
Project description:We demonstrated canine influenza virus (H3N2) pathogenicity to dogs using microarray analysis. Many genes related to innate immunity, such as toll-like receptors, immune cells of natural killer cells, macrophages, neutrophils, nitric oxide and reactive oxygen species, and interferon, were induced. RNA was extracted from canine influenza virus H3N2-infected dogs. The lung RNA of uninfected dogs was used as a negative control. We compared gene expression levels between infected and uninfected dogs using microarray analysis.
Project description:This research focus primarily on the interaction between influenza virus and endothelial cell, then we used microarrays to observe global patterns of gene expression in Human Umbilical Vein Endothelial Cells after influenza virus infection and offer further insight into the interaction between endothelial cells and influenza viruses. We used microarrays to detail the global programme of gene expression and identified distinct classes of up-regulated genes during this process.
Project description:This research focus primarily on the interaction between influenza virus and endothelial cell, then we used microarrays to observe global patterns of gene expression in Human Umbilical Vein Endothelial Cells after influenza virus infection and offer further insight into the interaction between endothelial cells and influenza viruses. We used microarrays to detail the global programme of gene expression and identified distinct classes of up-regulated genes during this process. Human Umbilical Vein Endothelial Cells were selected at an early stage for RNA extraction and hybridization on Affymetrix microarrays. Then, we analysed the selected genes at expression level.
Project description:We demonstrated canine influenza virus (H3N2) pathogenicity to dogs using microarray analysis. Many genes related to innate immunity, such as toll-like receptors, immune cells of natural killer cells, macrophages, neutrophils, nitric oxide and reactive oxygen species, and interferon, were induced.
Project description:The outcome of viral infection is extremely heterogeneous at the cellular level, and infected cells only sometimes activate innate immunity. Here we assess how the genetic variation inherent in viral populations contributes to this heterogeneity. We do this by developing a new approach to determine both the cellular transcriptome and full-length sequences of all viral genes in single influenza-infected cells. Infections that activate an innate-immune response in single cells are associated with viral defects that include amino-acid mutations, internal deletions, and failure to express key genes. However, immune activation remains stochastic in cells infected by virions with these defects, and sometimes occurs even in cells infected by virions that express unmutated copies of all genes. Our work shows that the genetic variation present in influenza virus populations substantially contributes to but does not fully explain the heterogeneity in infection outcome and immune activation in single infected cells.
