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 influenza A(H1N1)pdm09 virus caused a global flu pandemic in 2009 and contributes to seasonal epidemics. Different treatment and prevention options for influenza have been developed and applied with limited success. Here we report that an Akt inhibitor MK2206 possesses potent antiviral activity against influenza A(H1N1)pdm09 virus in vitro. We showed that MK2206 blocks the entry of different A(H1N1)pdm09 strains into cells. Moreover, MK2206 prevented A(H1N1)pdm09-mediated activation of cellular signaling pathways and the development of cellular immune responses. Importantly, A(H1N1)pdm09 virus was unable to develop resistance to MK2206. Thus, MK2206 is a potent anti-influenza A(H1N1)pdm09 agent.
Project description:An influenza A microarray was used to type influenza A H1N1 specimens collected in Washington State and the results compared with identification by both culture and real time RT PCR. The microarray was more sensitive than conventional influenza testing. Cluster analysis of the microarray data discriminated specimens into distinct clades. Specimens from two pediatric decedents formed a unique clade upon H1 analysis. Keywords: Comparative genome study; Influenza A strains; Subtype H1N1
Project description:To determine whether differential expression of cellular microRNAs plays a role in the host response to Influenza A (H1N1) infection, we have employed the Agilent miRNA microarray (V3) as a discovery platform to identify microRNAs between the critically ill Patients with Influenza A (H1N1) and the healthy controls.
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:The influenza A(H1N1)pdm09 virus caused a global flu pandemic in 2009 and contributes to seasonal epidemics. Different treatment and prevention options for influenza have been developed and applied with limited success. Here we report that an Akt inhibitor MK2206 possesses potent antiviral activity against influenza A(H1N1)pdm09 virus in vitro. We showed that MK2206 blocks the entry of different A(H1N1)pdm09 strains into cells. Moreover, MK2206 prevented A(H1N1)pdm09-mediated activation of cellular signaling pathways and the development of cellular immune responses. Importantly, A(H1N1)pdm09 virus was unable to develop resistance to MK2206. Thus, MK2206 is a potent anti-influenza A(H1N1)pdm09 agent. Total RNA obtained from NCI-H1666 cells, which are non-small cell lung cancer cell line. NCI-H1666 cells were non- or MK2206-treated (10 μM) and mock- or virus-infected (A/Helsinki/p14/2009) at moi of 3.
Project description:Influenza A virus is a kind of single negative-stranded RNA virus which belongs to the Orthomyxoviridae family. It can cause localized outbreak or worldwide epidemic in a short time for its great contagiosity, fast spread speed and a wide range of host, and H1N1 influenza virus is a strong pathogenic subtype of influenza A virus. Influenza A virus infection has been shown to alter miRNA expression both in cultured cells and in animal models. We used microRNA microarrays to detail the programme of microRNA expression and identified distinct classes of differentially regulated microRNAs during this process.
Project description:An influenza A microarray was used to type influenza A H1N1 specimens collected in Washington State and the results compared with identification by both culture and real time RT PCR. The microarray was more sensitive than conventional influenza testing. Cluster analysis of the microarray data discriminated specimens into distinct clades. Specimens from two pediatric decedents formed a unique clade upon H1 analysis. Keywords: Comparative genome study; Influenza A strains; Subtype H1N1 23 influenza A H1N1 specimens collected in Washington State were subtyped by microarray and data was compared with identification by both culture and real time RT PCR.
