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Acute host transcriptonal response to r1918 influenza and r1918 influenza containing the NS1 gene from A/Texas/36/91 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 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).

ORGANISM(S): Homo sapiens

PROVIDER: GSE37951 | GEO | 2012/05/14

SECONDARY ACCESSION(S): PRJNA165829

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

2012-05-14 | GSE37829 | GEO

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 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

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

The 1918 PB2 protein, not HA, enhances the virulence of an avian influenza virus closely related to the 1918 pandemic virus through the inhibition of wnt signaling.

2015-12-31 | GSE70502 | GEO

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

Role for HA and the viral RNA polymerase complex in the virulence of the 1918 influenza virus

Project description:The goal of this experiment was to examine the biological properties of reassortant viruses between the 1918 virus and a contemporary human H1N1 virus to determine the role of hemagglutinin (HA) and the viral RNA polymerase complex of 1918 virus toward pathogenesis and abberant host responses in mice.

2013-02-23 | GSE44595 | GEO

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.

2011-11-01 | GSE33351 | GEO

The 1918 PB2 protein, not HA, enhances the virulence of an avian influenza virus closely related to the 1918 pandemic virus through the inhibition of wnt signaling.

Project description:The purpose of this experiment was to understand the pathogenic role of individual 1918 genes on the host response to the 1918 pandemic influenza virus. We examined reassortant avian viruses nearly identical to the pandemic 1918 virus (1918-like avian virus) carrying either the 1918 HA or PB2 gene. Both genes enhanced 1918-like avian virus replication, but only the mammalian host adaptation of the 1918-like avian virus through reassortment of the 1918 PB2 led to increased lethality in mice. We demonstrate that 1918 PB2 enhances immune and inflammatory responses concomitant with increased cellular infiltration in the lung. We also show that 1918 PB2 expression results in the repression of both canonical and non-canonical Wnt signaling pathways which are crucial for inflammation mediated lung regeneration and repair. Five- to six-week-old female BALB/c mice (Jackson Laboratory) were used for the experiments. Isoflurane-anesthetized mice were intranasally inoculated with tenfold serial dilutions (three mice per dilution) of 1918, 1918-like avian, 1918 PB2/avian and 1918 HA/avian viruses. The dose required to kill 50% of mice (MLD50) was calculated using the Reed-Muench method. For analysis of virus growth and microarray profiling mice were intranasally inoculated with 10^4 PFU of virus (n=4/virus/timepoint) or PBS (n=3/timepoint). At days 1, 2 and 4 after infection, lungs were harvested from the infected mice. Lungs were processed for RNA extraction for microarray studies and virus titer determination.

2015-12-31 | E-GEOD-70502 | 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

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