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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Integrated Clinical, Pathologic, Virologic, and Transcriptomic Analysis of H5N1 Influenza Virus-Induced Viral Pneumonia in the Rhesus Macaque

ABSTRACT: Viral pneumonia has been frequently reported during early stages of influenza virus pandemics and in many human cases of highly pathogenic avian influenza (HPAI) H5N1 virus infection. To better understand the pathogenesis of this disease, we produced non-lethal viral pneumonia in rhesus macaques by using an HPAI H5N1 virus (A/Anhui/2/2005; referred to as Anhui/2). Infected macaques were monitored for 14 days, and tissue samples were collected at 6 time points for virologic, histopathologic and transcriptomic analyses. Thirteen colony-bred male or female rhesus macaques (Macaca mulatta), aged from 2.5 to 3.5 years and ranging in weight from 2.8 to 4.4 kg, were used for experiments. Twelve macaques were individually infected intratracheally with 10^7 EID50 of Anhui/2 in 4 ml of phosphate-buffered saline (PBS). At 6 h, 12 h, 1 d, 3 d, 6 d, and 14 d post-infection (p.i.), two animals per time-point were euthanized under anesthesia and necropsies were performed. Lung samples were collected and stored in RNAlater (Ambion, Austin, USA) at -80M-BM-0C for RNA analyses. The remaining macaque (mock-infected) was inoculated with 4 ml of PBS intratracheally and euthanized at 6 h p.i. Lung tissues from the mock-infected animal were collected and stored as described.

ORGANISM(S): Macaca mulatta

SUBMITTER: Richard Green

PROVIDER: E-GEOD-37149 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Integrated Clinical, Pathologic, Virologic, and Transcriptomic Analysis of H5N1 Influenza Virus-Induced Viral Pneumonia in the Rhesus Macaque

Project description:Viral pneumonia has been frequently reported during early stages of influenza virus pandemics and in many human cases of highly pathogenic avian influenza (HPAI) H5N1 virus infection. To better understand the pathogenesis of this disease, we produced non-lethal viral pneumonia in rhesus macaques by using an HPAI H5N1 virus (A/Anhui/2/2005; referred to as Anhui/2). Infected macaques were monitored for 14 days, and tissue samples were collected at 6 time points for virologic, histopathologic and transcriptomic analyses.

2012-04-11 | GSE37149 | GEO

Lung proteome analysis of highly pathogenic avian influenza virus (H5N1) infection progression in chicken

Project description:This study is planned to characterize the proteome profile of HPAI H5N1 virus infected chicken lung tissues to identify the molecular pathogenesis and proteomic determinant associate with disease progression in susceptible host.

2022-03-02 | PXD010358 | Pride

Host Regulatory Network Response to Infection with Highly Pathogenic H5N1 Avian Influenza Virus

Project description:Over the last decade, more than half of humans infected with highly pathogenic avian influenza (HPAI) H5N1 viruses have died, and yet virus-induced host signaling has yet to be clearly elucidated. Airway epithelia are known to produce inflammatory mediators that contribute to HPAI H5N1-mediated pathogenicity, but a comprehensive analysis of the host response in this cell type is lacking. Here, we leveraged a systems biology method called weighted gene correlation network analysis (WGCNA) to identify and statistically validate signaling sub-networks that define the dynamic transcriptional response of human bronchial epithelial cells after infection with influenza A/Vietnam/1203/2004 (H5N1, VN1203). A detailed examination of two sub-networks involved in the immune response and keratin filament formation revealed potential novel mediators of HPAI H5N1 pathogenesis, and additional experiments validated upregulation of these transcripts in response to VN1203 infection in C57BL/6 mice. Using emergent network properties, we provide fresh insight into the host response to HPAI H5N1 virus infection, and identify novel avenues for perturbation studies and potential therapeutic intervention of fatal HPAI H5N1 disease. Calu-3 cells were infected with VN1203 influenza virus and profiled at 0, 3, 7, 12, 18, and 24 hours post infection. There are 3 mock and infected replicates for each time point.

2011-09-01 | E-GEOD-28166 | biostudies-arrayexpress

Characterizing the transcriptomic response of mice infected with A/Anhui/01/2013 (H7N9), A/Netherlands/219/2003 (H7N7), and A/Vietnam/1203/2004 (H5N1), and a pandemic H1N1 human virus, A/Mexico/4482/2007 (H1N1)

Project description:Modulating the host response is a promising approach to treating influenza, a virus whose pathogenesis is determined in part by the host response it elicits. Though the pathogenicity of emerging H7N9 influenza virus has been reported in several animal models, these studies have not included a detailed characterization of the host response following infection. To this end, we characterized the transcriptomic response of BALB/c mice infected with H7N9 (A/Anhui/1/2013) virus and compared it to the responses induced by H5N1 (A/Vietnam/1203/2004), H7N7 (A/Netherlands/219/2003) or H1N1 (A/Mexico/4482/2009) viruses. We found that responses to the H7 subtype viruses were intermediate to those elicited by H5N1 and H1N1 early in infection, but that they evolved to resemble the H5N1 response as infection progressed. H5N1, H7N7 and H7N9 viruses were pathogenic in mice, and this pathogenicity correlated with increased cytokine response, decreased lipid metabolism and decreased coagulation signaling. This three-pronged signature has previously been observed in mice infected with pathogenic H1N1 strains such as the 1918 virus, indicating that it may be predictive of pathogenicity across multiple influenza strains. Groups of 6- to 8-week-old BALB/c mice were infected with either A/Anhui/01/2013 (H7N9), A/Netherlands/219/2003 (H7N7), A/Vietnam/1203/2004 (H5N1), or pandemic H1N1 human virus, A/Mexico/4482/2007 (H1N1). Infections were done at 10^5 PFU or time-matched mock infected. Time points were 1, 3 and 5 d.p.i. There were 4-5 infected and 3 mock infected animals/time point. Lung samples were collected for virus load and transcriptional analysis. Weight loss and animal survival were also monitored.

2014-05-27 | E-GEOD-54048 | biostudies-arrayexpress

Neutrophil extracellular traps and alveolar barrier disruption contribute to varicella pneumonia pathology

Project description:Varicella pneumonia is the most common and severe complication of primary varicella-zoster virus (VZV) infection in adults. Pathogenesis of varicella pneumonia is largely unknown, mainly due to limited availability of clinical specimens and lack of appropriate VZV animal models. Simian varicella virus (SVV) infection of nonhuman primates closely recapitulates clinical and pathogenic features of human VZV disease. This study aimed to elucidate the virus and host factors that contribute to the pathogenesis of varicella pneumonia. The deposited data present changes in gene expression in the lung of SVV-infected cynomolgus macaques (Macaca fascicularis) at 3, 6 and 9 days after infection, and mock-infected control macaques at 3 days after infection.

2020-09-01 | E-MTAB-8485 | biostudies-arrayexpress

Host Regulatory Network Response to Infection with Highly Pathogenic H5N1 Avian Influenza Virus

2011-09-02 | GSE28166 | GEO

Expression data of influenza A infected human macrophages

Project description:Human disease caused by highly pathogenic avian influenza (HPAI) H5N1 can lead to a rapidly progressive viral pneumonia leading to acute respiratory distress syndrome. There is increasing evidence suggests a role for virus-induced cytokine dysregulation in contributing to the pathogenesis of human H5N1 disease. The key target cells for the virus in the lung are the alveolar epithelium and alveolar macrophages, and previous data has shown that compared to seasonal human influenza viruses, equivalent infecting doses of H5N1 viruses markedly up-regulate pro-inflammatory cytokines in both primary cell types in vitro. The dysregulation of H5N1-induced host responses is therefore important for understanding the viral pathogenesis. We used microarrays to analyze and compare the gene expression profiles in primary human macrophages after influenza A virus infection. Peripheral-blood leucocytes were separated from buffy coats of three healthy blood donors and cells were differentiated for 14 days before use. Differentiated macrophages were infected with H1N1 and H5N1 at a multiplicity of infection (MOI) of two. Total RNA was extracted from cells after 1, 3, and 6h post-infection, and gene expression profiling was performed using an Affymetrix Human Gene 1.0 ST microarray platform.

2009-10-31 | E-GEOD-18816 | biostudies-arrayexpress

Quantitative proteomic analysis of duck lung tissue during infection of avian influenza

Project description:Ducks and wild aquatic birds are the natural reservoirs of avian influenza viruses. However, the host proteome response that causes disease in vivo during infection by the highly pathogenic avian influenza (HPAI) H5N1 virus is still not well understood. In the present study, we compared the proteome response in Muscovy duck lung tissue during 3 day of infection with either a highly virulent or an avirulent H5N1 virus. During infection, proteins involved in immune response of neutrophils and size of cells were increased markedly in the lung by the virulent strain, while the avirulent strain evoked a distinct response, characterized by an increase in proteins involved in cell movement, maturation of dendritic cells, adhesion of phagocytes, and immune response of macrophages.

2022-08-22 | PXD002719 | Pride

Expression data of influenza A infected human macrophages

2009-10-31 | GSE18816 | GEO

Transcriptomic characterization of the novel avian-origin influenza A (H7N9) virus: specific and intermediate host-response between avian (H5N1 and H7N7) and human (H3N2) viruses.

Project description:A novel avian-origin H7N9 influenza A virus (IAV) emerged in China in early 2013 causing mild to lethal human respiratory infections. H7N9 originated from multiple reassortment events between avian viruses and carries genetic markers of human adaptation. Determining whether H7N9 induces a host-response closer to human or avian IAV is important to better characterize this emerging virus. Here we compared the human lung epithelial cell response to infection with A/Anhui/01/13 (H7N9) or highly pathogenic avian-origin H5N1, H7N7, or human seasonal H3N2 IAV. Here, polarized confluent monolayers of Calu-3 cells were infected apically with the avian-origin IAVs A/Anhui/01/2013 (H7N9) [Anhui01], A/Netherland/219/2003 (H7N7) [NL219], A/Vietnam/1203/2004 (H5N1) [VN1203], or a human seasonal virus A/Panama/2007/1999 (H3N2) [Pan99] at an MOI of 1. Time-matched mocks were also included using the same cell stock as the rest of the samples. Culture medium (same as what the virus stock is in) was used for the mock infections. Quadruplicate wells were infected for each virus/timepoint. Measured timepoints were 3, 7, 12 and 24 hours post-inoculation and the RNA was used for transcriptional analysis via microarray.

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