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RNAseq analysis of B6-Mx1(r) and D2-Mx1(r) mice infected with PR8 virus

ABSTRACT: Gene expression changes in the lung was studied by RNAseq Results: Strong differences in the immune response between the two mouse strains

ORGANISM(S): Mus musculus

PROVIDER: GSE165355 | GEO | 2021/01/23

REPOSITORIES: GEO

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RNAseq analysis of B6-Mx1(r) and D2-Mx1(r) mice infected with PR8 virus, map to mm11

Project description:Strong differences in the immune response between the two mouse strains were found

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RNAseq analysis of B6-Mx1(r) and D2-Mx1(r) mice infected with PR8 virus

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RNAseq analysis of B6-Mx1(r) and D2-Mx1(r) mice infected with PR8 virus, map to mm11

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RNAseq analysis of BXD mouse strains infected with PR8M virus

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RNA-seq influenza infected B6 & D2 mice

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RNA-seq influenza infected B6 & D2 mice

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RNAseq analysis of CC strains after influenza A virus infection identifies genetic control of the host response

Project description:Gene expression changes in the lung was studied by RNAseq in different CC mouse strains infected with influenza A virus. Results: Strong differences between the genetically CC mouse strains can be observed in the activation of host defense genes. These differences can be related to genetic variants in the genome of the CC strains. Furthermore, different strains exhibit variant susceptibility to infections (body weight loss and survival). These differences can be correlated to differences in gene expression profiles.

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RNAseq analysis of BXD mouse strains infected with PR8M virus

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Serial histopathological examination of the lungs of mice infected with influenza A virus PR8 strain.

Project description:Avian influenza H5N1 and pandemic (H1N1) 2009 viruses are known to induce viral pneumonia and subsequent acute respiratory distress syndrome (ARDS) with diffuse alveolar damage (DAD). The mortality rate of ARDS/DAD is extremely high, at approximately 60%, and no effective treatment for ARDS/DAD has been established. We examined serial pathological changes in the lungs of mice infected with influenza virus to determine the progress from viral pneumonia to ARDS/DAD. Mice were intranasally infected with influenza A/Puerto Rico/8/34 (PR8) virus, and their lungs were examined both macro- and micro-pathologically every 2 days. We also evaluated general condition, survival rate, body weight, viral loads in lung, and surfactant proteins in serum. As a result, all infected mice died within 9 days postinfection. At 2 days postinfection, inflammation in alveolar septa, i.e., interstitial pneumonia, was observed around bronchioles. From 4 to 6 days postinfection, interstitial pneumonia with alveolar collapse expanded throughout the lungs. From 6 to 9 days postinfection, DAD with severe alveolar collapse was observed in the lungs of all of dying and dead mice. In contrast, DAD was not observed in the live infected-mice from 2 to 6 days postinfection, despite their poor general condition. In addition, histopathological analysis was performed in mice infected with a dose of PR8 virus which was 50% of the lethal dose for mice in the 20-day observation period. DAD with alveolar collapse was observed in all dead mice. However, in the surviving mice, instead of DAD, glandular metaplasia was broadly observed in their lungs. The present study indicates that DAD with severe alveolar collapse is associated with death in this mouse infection model of influenza virus. Inhibition of the development of DAD with alveolar collapse may decrease the mortality rate in severe viral pneumonia caused by influenza virus infection.

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Project description:Gene expression changes in the blood was studied by RNAseq Results: Strong differential host reponse after infection with influenza virus compared to healthy controls project SIG_2020

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