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Acute host transcriptonal response to A/Texas/36/91 influenza and A/Texas/36/91 influenza containing the NS1 gene from r1918 in A549 cells

ABSTRACT: The “Spanish influenza” of 1918 claimed an unprecedented number of lives, yet the determinants of virulence for this virus are still not fully understood. Here, we used functional genomics and an in vitro human lung epithelial cell infection model to define the global host transcriptional response to the eight-gene 1918 virus. To better understand the role of the 1918 virus NS1 gene, we evaluated the host response to A/Texas/36/91 (a seasonal isolate of human influenza virus) and a reassortant of A/Texas/36/91 containing the 1918 NS1 gene.

ORGANISM(S): Homo sapiens

PROVIDER: GSE37829 | GEO | 2012/05/14

SECONDARY ACCESSION(S): PRJNA165851

REPOSITORIES: GEO

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Acute host transcriptonal response to A/Texas/36/91 influenza and A/Texas/36/91 influenza containing the NS1 gene from r1918 in A549 cells

Project description:The M-bM-^@M-^\Spanish influenzaM-bM-^@M-^] of 1918 claimed an unprecedented number of lives, yet the determinants of virulence for this virus are still not fully understood. Here, we used functional genomics and an in vitro human lung epithelial cell infection model to define the global host transcriptional response to the eight-gene 1918 virus. To better understand the role of the 1918 virus NS1 gene, we evaluated the host response to A/Texas/36/91 (a seasonal isolate of human influenza virus) and a reassortant of A/Texas/36/91 containing the 1918 NS1 gene. A549 cells were infected at a MOI=2 with either A/Texas/36/91 (Tx/91) or A/Texas/36/91 (Tx/91) containing the NS1 gene from r1918 influenza. Virus was allowed to bind to cells for 1 h at 4M-BM-0C in serum-free infection medium supplemented with trypsin (1 g/ml). Mock-infected cells were treated with allantoic fluid instead of virus. Three replicate wells were used for each infection condition at each time point. Cells were harvested for array analysis at 2, 6, and 24hr post-infection. Cells from three individual cultures were pooled for each condition for microarray.

2012-05-13 | E-GEOD-37829 | biostudies-arrayexpress

Acute host transcriptonal response to r1918 influenza and r1918 influenza containing the NS1 gene from A/Texas/36/91 in A549 cells

Project description:The “Spanish influenza” of 1918 claimed an unprecedented number of lives, yet the determinants of virulence for this virus are still not fully understood. Here, we used functional genomics and an in vitro human lung epithelial cell infection model to define the global host transcriptional response to the eight-gene 1918 virus. To better understand the role of the 1918 virus NS1 gene, we also evaluated the host response to fully reconstructed 1918 and reassortant 1918 virus containing the NS1 gene from A/Texas/36/91 (a seasonal isolate of human influenza virus). A549 cells were infected with either recombinant 1918 influenza, a chimeric virus that contained seven genes from recombinant 1918 and the NS1 from A/Texas/36/91 (Tx/91), or mock. Cells were harvested for microarray analysis at 2, 6, and 24hr following infection.

2012-05-13 | E-GEOD-37951 | biostudies-arrayexpress

Acute host transcriptonal response to r1918 influenza and r1918 influenza containing the NS1 gene from A/Texas/36/91 in A549 cells

2012-05-14 | GSE37951 | GEO

The NS1 protein of influenza A virus suppresses interferon-regulated activation of antigen-presentation and immune-proteasome pathways

2012-07-10 | GSE39200 | GEO

The NS1 protein of influenza A virus suppresses interferon-regulated activation of antigen-presentation and immune-proteasome pathways

Project description:The NS1 protein of influenza virus counters host antiviral defences primarily by antagonizing the type I interferon (IFN) response. Both the N-terminal dsRNA-binding domain and the C-terminal effector domain are required for optimal suppression of host responses during infection. To better understand the regulatory role of the NS1 effector domain, we used an NS1-truncated mutant virus derived from human H1N1 influenza isolate A/Texas/36/91 (Tx/91) and assessed global transcriptional profiles from two independent human lung cell-culture models. Primary human tracheobronchial epithelial (HTBE) cells were washed and infected with 4×10^6 p.f.u. Tx/91 or Tx/91 NS1 : 1–126 viruses per filter (m.o.i. of 20) for 1 h at 37 °C. Three replicate wells were infected for each condition per time point. Allantoic fluid was used for mock treatments. At 9.5 and 25 h p.i., cells were collected and resuspended in TRIzol reagent (Invitrogen) for total RNA extraction. A549 cells were infected with Tx/91 or Tx/91 NS1 : 1–126 viruses at an m.o.i. of 2 for 1 h at 4 °C. Three replicate wells were infected for each condition per time point. Allantoic fluid was used for mock treatments. A549 cells were collected and lysed in solution D (4 M guanidinium thiocyanate, 25 mM sodium citrate, 0.5 % sarcosyl, 0.1 M β-mercaptoethanol) at 12 and 24 h p.i. for total RNA extraction.

2012-07-09 | E-GEOD-39200 | biostudies-arrayexpress

Early and sustained innate immune response defines pathology and death in nonhuman primates infected by highly pathogenic influenza virus.

Project description:This study revealed important similarities but also critical differences between the H5N1 and 1918-reassortant viruses, highlighting aspects of the host–pathogen interface caused by highly virulent influenza viruses. Animals assigned to 4 experimental groups (n = 8) matched for age, weight, and sex, were inoculated by intratracheal, intranasal, tonsillar, and conjunctival routes with a total of 107 pfu of A/Vietnam/1203/2004 (H5N1) virus, A/Texas/36/91 (H1N1) virus or reassortants of this virus containing either 2 (HA, NA) or 3 (HA, NA, NS) genes from the 1918 virus. Two animals per group were scheduled for sacrifice on days 1, 2, 4, and 7. Two additional animals were used as uninfected control animals and killed on day 7. Oligoarray analyses consisted of comparing array profiles of individual lung samples (with representative pathology and degree of infection) from infected animals to pooled equal masses of mRNA from all lung lobes of 7 reference cynomolgus macaques obtained through the tissue program of the University of Washington National Primate Research Center. There are 2 technical array replicates fro each sample.

2011-11-01 | E-GEOD-33351 | biostudies-arrayexpress

Influenza virus infection causes global RNAPII termination defects

Project description:Viral infection perturbs host cells and can be used to uncover host regulatory mechanisms controlling both cell response and homeostasis. Here, using cell biological, biochemical and genetic tools, we reveal that influenza virus infection induces global transcriptional defects at the 3’-end of active host genes and RNA polymerase II (RNAPII) run-through into extragenic regions. This effect induces the biogenesis of aberrant RNAs (3’-extensions and host gene fusions) which ultimately causes global transcriptional downregulation of physiological transcripts, an effect that impacts antiviral response and virulence. We show that this phenomenon occurs with multiple strains of influenza virus and it is dependent on influenza NS1 protein expression. Mechanistically, pervasive RNAPII run-through can be modulated by SUMOylation of an intrinsically disordered region (IDR) of the NS1 expressed by the 1918 pandemic influenza virus. SUMOylation increases NS1 partitioning in nuclear granules and interference with the host transcriptional apparatus which result in augmentation of termination defects and a concomitant increase in global host gene shut off. Our data identify a general strategy used by influenza virus to suppress host gene expression and indicate that polymorphisms in IDRs of viral proteins, along with human genetic variation in enzymes that metabolize post-translational modifications, can determine the outcome of an infection. We thus propose that analysis of strain-specific determinant of pathogenesis can shed light on the molecular basis of virulence.

2018-09-05 | GSE103604 | GEO

NS1-mediated inhibition of c-Abl results in acute lung injury and priming for bacterial co-infections; insights into 1918 H1N1 pandemic

Project description:NS1 proteins from avian influenza viruses like the 1918 pandemic NS1 are capable of inhibiting the key signaling integrator c-Abl (Abl1), resulting in massive cytopathic cell alterations. In the current study, we addressed the consequences of NS1-mediated alteration of c-Abl on acute lung injury and pathogenicity. Comparing isogenic strains that differ only in their ability to inhibit c-Abl, we observed elevated pathogenicity for the c-Abl-inhibiting virus. NS1-mediated block of c-Abl resulted in severe lung pathology and massive edema formation and facilitated secondary bacterial pneumonia. This phenotype was independent of differences in replication and immune responses, defining it as an NS1 virulence mechanism distinct from its canonical functions. Microarray analysis revealed extensive down-regulation of genes involved in cell integrity and vascular endothelial regulation. In conclusion, NS1 protein-mediated blockade of c-Abl signaling drives acute lung injury and primes for bacterial co-infections revealing potential insights into the pathogenicity of the 1918 pandemic virus. Lung transcription analysis of Influenza A virus infected mice.

2014-11-03 | E-GEOD-62169 | biostudies-arrayexpress

1918 pandemic influenza virus and pneumococcus co-infection results in activation of coagulation and widespread pulmonary microvascular thrombosis in mice and humans

Project description:To study the effects of secondary bacterial infection during 1918 pandemic H1N1 influenza virus infection, BALB/c mice were inoculated with the fully reconstructed 1918 influenza virus followed by inoculation with pneumococcus 72h later. To study the effects of secondary bacterial infection during 1918 pandemic H1N1 influenza virus infection, BALB/c mice were inoculated with the fully reconstructed 1918 influenza virus followed by inoculation with pneumococcus 72h later.

2015-09-20 | E-GEOD-70445 | biostudies-arrayexpress

1918 pandemic influenza virus and pneumococcus co-infection results in activation of coagulation and widespread pulmonary microvascular thrombosis in mice and humans

2015-09-20 | GSE70445 | GEO

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