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IM010 - Infection with A/Vietnam/1203/04 H5N1 influenza virus of C57BL/6J mice, IDO1 KO mice or TNFRSF1B KO mice

ABSTRACT: Comparison of the host response to VN1203 infection in three different strains of mice: Wild-type C57BL/6J mice, IDO1 KO mice and TNFRSF1B KO.

ORGANISM(S): Mus musculus

PROVIDER: GSE40792 | GEO | 2012/09/12

SECONDARY ACCESSION(S): PRJNA174988

REPOSITORIES: GEO

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IM010 - Infection with A/Vietnam/1203/04 H5N1 influenza virus of C57BL/6J mice, IDO1 KO mice or TNFRSF1B KO mice

Project description:Comparison of the host response to VN1203 infection in three different strains of mice: Wild-type C57BL/6J mice, IDO1 KO mice and TNFRSF1B KO. Groups of 6-week-old mice were infected with A/Vietnam/1203/04 H5N1 influenza virus at a dose of 10^3 PFU or mock infected. Mice were euthanized on days 2 and 6 post-infection to measure virus load and isolate samples for measurement of virus load, lung pathology, transcriptional analysis and proteomics analysis. Mock-infected animals were also harvested at each time point. Mice were weighed every 24 hours to measure general disease progression and any mouse approaching 30% weight loss was euthanized.

2012-09-12 | E-GEOD-40792 | biostudies-arrayexpress

ICL0011 - Host response in human Calu-3 cells to infection with A/Vietnam/1203-CIP048_RG3/2004 (H5N1) (PB1-F2 deletion), A/Vietnam/1203-CIP048_RG3/2004 (H5N1) (PB2-627E mutant) or WT: A/Vietnam/1203/2004 (H5N1)

2013-01-05 | GSE43203 | GEO

Project description:Differential expression was determined in Calu-3 cells between mock infected and infection with one of 3 Influenza viruses (wild-type VN1203, VN1203 mutant PB1-F2del, VN1203 mutant PB2-627E) at different times post infection. Purpose: To obtain samples for transcriptional analysis in triplicate using the VN1203 pathogenicity mutants PB1-F2del and PB2-627E. Overview of Experiment: . Time Points: 0, 3, 7, 12, 18 and 24 hrs post infection. . There are two time points for wild type VN1203. . Done in triplicate. . Triplicates are defined as 3 different wells, plated at the same time using the same cell stock for all replicates. . Time-matched mocks were done in triplicate from the same cell stock as the rest of the samples. . Culture medium (the same as what the virus stock is in) was used for the mock infections. Calu-3 cells were infected with A/Vietnam/1203-CIP048_RG3/2004 (H5N1) (PB1-F2 deletion), A/Vietnam/1203-CIP048_RG3/2004 (H5N1) (PB2-627E mutant) or mock infected and samples were collected at 0, 3, 7, 12, 18 and 24 hpi. Calu-3 cells were infected with WT: A/Vietnam/1203/2004 (H5N1) and samples were collected at 7 and 24 hpi. There are 3 mock and 3 infected replicates for each time point. Expression profiles were determined.

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Injectable peramivir mitigates disease and promotes survival in ferrets and mice infected with the highly virulent influenza virus, A/Vietnam/1203/04 (H5N1).

Project description:The post-exposure therapeutic efficacy of injectable peramivir against highly pathogenic avian influenza type A H5N1 was evaluated in mice and in ferrets. Seventy to eighty percent of the H5N1-infected peramivir-treated mice, and 70% in the oseltamivir treated mice survived the 15-day study period, as compared to 36% in control (vehicle) group. Ferrets were infected intranasally with H5N1 followed by treatment with multiple doses of peramivir. In two of three trials, a statistically significant increase in survival over a 16-18 day period resulted from peramivir treatment, with improved survival of 40-64% in comparison to mock-treated or untreated animals. Injected peramivir mitigates virus-induced disease, reduces infectious virus titers in the lungs and brains and promotes survival in ferrets infected intranasally with this highly neurovirulent isolate. A single intramuscular peramivir injection protected mice against severe disease outcomes following infection with highly pathogenic avian influenza and multi-dose treatment was efficacious in ferrets.

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Project description:Differential expression was determined in Calu-3 cells between mock infected and infection with NS1trunc124: A/Vietnam/1203-CIP048_RG4/2004 (H5N1) or WT: A/Vietnam/1203/2004 (H5N1) at different times post infection. Purpose: To obtain samples for transcriptional analysis in triplicate using the VN1203 pathogenicity mutant NS1-trunc124. Overview of Experiment: . Time Points: 0, 3, 7, 12, 18 and 24 hrs post infection. . Done in triplicate. . Triplicates are defined as 3 different wells, plated at the same time using the same cell stock for all replicates. . Time-matched mocks were done in triplicate from the same cell stock as the rest of the samples. . Culture medium (the same as what the virus stock is in) was used for the mock infections. Calu-3 cells were infected with NS1trunc124: A/Vietnam/1203-CIP048_RG4/2004 (H5N1) or mock infected and samples were collected at 0, 3, 7, 12, 18 and 24 hpi. Calu-3 cells were infected with WT: A/Vietnam/1203/2004 (H5N1) and samples were collected at 7 and 24 hpi. There are 3 mock (2 included here) and 3 infected replicates for each time point. Expression profiles were determined.

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Neuraminidase inhibitor-resistant recombinant A/Vietnam/1203/04 (H5N1) influenza viruses retain their replication efficiency and pathogenicity in vitro and in vivo.

Project description:Effective antiviral drugs are essential for early control of an influenza pandemic. It is therefore crucial to evaluate the possible threat posed by neuraminidase (NA) inhibitor-resistant influenza viruses with pandemic potential. Four NA mutations (E119G, H274Y, R292K, and N294S) that have been reported to confer resistance to NA inhibitors were each introduced into recombinant A/Vietnam/1203/04 (VN1203) H5N1 influenza virus. For comparison, the same mutations were introduced into recombinant A/Puerto Rico/8/34 (PR8) H1N1 influenza virus. The E119G and R292K mutations significantly compromised viral growth in vitro, but the H274Y and N294S mutations were stably maintained in VN1203 and PR8 viruses. In both backgrounds, the H274Y and N294S mutations conferred resistance to oseltamivir carboxylate (50% inhibitory concentration [IC(50)] increases, >250-fold and >20-fold, respectively), and the N294S mutation reduced susceptibility to zanamivir (IC(50) increase, >3.0-fold). Although the H274Y and N294S mutations did not compromise the replication efficiency of VN1203 or PR8 viruses in vitro, these mutations slightly reduced the lethality of PR8 virus in mice. However, the VN1203 virus carrying either the H274Y or N294S mutation exhibited lethality similar to that of the wild-type VN1203 virus. The different enzyme kinetic parameters (V(max) and K(m)) of avian-like VN1203 NA and human-like PR8 NA suggest that resistance-associated NA mutations can cause different levels of functional loss in NA glycoproteins of the same subtype. Our results suggest that NA inhibitor-resistant H5N1 variants may retain the high pathogenicity of the wild-type virus in mammalian species. Patients receiving NA inhibitors for H5N1 influenza virus infection should be closely monitored for the emergence of resistant variants.

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Lysosome-enriched fractions from the liver of Cln8 KO mice and WT mice

Project description:Lysosome-enriched fractions from the liver of Cln8 KO mice and WT mice. Included are four datasets: 1. Lysosome-enriched fraction from the liver of Cln8 KO mice, replicate 1 (CLN8_KO_1). 2. Lysosome-enriched fraction from the liver of Cln8 KO mice, replicate 2 (CLN8_KO_2). 3. Lysosome-enriched fraction from the liver of WT mice, replicate 1 (WT_1). 4. Lysosome-enriched fraction from the liver of WT mice, replicate 2 (WT_2).

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Project description:Comparing the host response of C57BL/6J mice to Tnfrsf1b knockouts in the same strain of mice.

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