10 results on '"Kawaoka, Yoshihiro"'
Search Results
2. Hypergraph models of biological networks to identify genes critical to pathogenic viral response
- Author
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Feng, Song, Heath, Emily, Jefferson, Brett, Joslyn, Cliff, Kvinge, Henry, Mitchell, Hugh D., Praggastis, Brenda, Eisfeld, Amie J., Sims, Amy C., Thackray, Larissa B., Fan, Shufang, Walters, Kevin B., Halfmann, Peter J., Westhoff-Smith, Danielle, Tan, Qing, Menachery, Vineet D., Sheahan, Timothy P., Cockrell, Adam S., Kocher, Jacob F., Stratton, Kelly G., Heller, Natalie C., Bramer, Lisa M., Diamond, Michael S., Baric, Ralph S., Waters, Katrina M., Kawaoka, Yoshihiro, McDermott, Jason E., and Purvine, Emilie
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- 2021
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3. Association of gut microbiota with the pathogenesis of SARS-CoV-2 Infection in people living with HIV.
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Ishizaka, Aya, Koga, Michiko, Mizutani, Taketoshi, Yamayoshi, Seiya, Iwatsuki-Horimoto, Kiyoko, Adachi, Eisuke, Suzuki, Yutaka, Kawaoka, Yoshihiro, and Yotsuyanagi, Hiroshi
- Subjects
SARS-CoV-2 ,GUT microbiome ,HIV-positive persons ,COVID-19 ,POST-acute COVID-19 syndrome ,NOSOLOGY - Abstract
Background: People living with HIV (PLWH) with chronic inflammation may have an increasing risk for coronavirus disease 2019 (COVID-19) severity; however, the impact of their gut microbiota on COVID-19 is not fully elucidated. Here, we analyzed the temporal changes in the gut microbiota composition of hospitalized severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-infected PLWH (PLWH-CoV) and their correlation with COVID-19 severity. Result: The 16S rRNA analysis results using stool samples (along the timeline from disease onset) from 12 hospitalized PLWH-CoV, whose median CD4 + T cell count was 671 cells/µl, were compared to those of 19 healthy people and 25 PLWH. Bacterial diversity in PLWH-CoV is not significantly different from that of healthy people and SARS-CoV-2 non-infected PLWH, but a significant difference in the microbiota diversity was observed in the classification according to the disease severity. Immediately after the disease onset, remarkable changes were observed in the gut microbiota of PLWH-CoV, and the changing with a decrease in some short-chain fatty acid-producing bacteria and an increase in colitis-related pathobiont. In the second week after disease onset, relative amounts of specific bacteria distinguished between disease severity. One month after the disease onset, dysbiosis of the gut microbiota persisted, and the number of Enterobacteriaceae, mainly Escherichia-Shigella, which is potentially pathogenic, increased and were enriched in patients who developed post-acute sequelae of COVID-19 (PASC). Conclusion: The changes in the gut microbiota associated with SARS-CoV-2 infection observed in PLWH in this study indicated a persistent decrease in SCFA-producing bacteria and an intestinal environment with an increase in opportunistic pathogens associated with enteritis. This report demonstrates that the intestinal environment in PLWH tends to show delayed improvement even after COVID-19 recovery, and highlights the importance of the dysbiosis associated with SARS-CoV-2 infection as a potential factor in the COVID-19 severity and the PASC in PLWH. [ABSTRACT FROM AUTHOR]
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- 2024
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4. Research article antibody induction and immune response in nasal cavity by third dose of SARS-CoV-2 mRNA vaccination.
- Author
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Ishizaka, Aya, Koga, Michiko, Mizutani, Taketoshi, Uraki, Ryuta, Yamayoshi, Seiya, Iwatsuki-Horimoto, Kiyoko, Yamamoto, Shinya, Imai, Masaki, Tsutsumi, Takeya, Suzuki, Yutaka, Kawaoka, Yoshihiro, and Yotsuyanagi, Hiroshi
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NASAL cavity ,IMMUNE response ,SARS-CoV-2 ,NASAL mucosa ,MESSENGER RNA ,IMMUNOGLOBULINS - Abstract
Background: The mucosa serves as the first defence against pathogens and facilitates the surveillance and elimination of symbiotic bacteria by mucosal immunity. Recently, the mRNA vaccine against SARS-CoV-2 has been demonstrated to induce secretory antibodies in the oral and nasal cavities in addition to a systemic immune response. However, the mechanism of induced immune stimulation effect on mucosal immunity and commensal bacteria profile remains unclear. Methods: Here, we longitudinally analysed the changing nasal microbiota and both systemic and nasal immune response upon SARS-CoV-2 mRNA vaccination, and evaluated how mRNA vaccination influenced nasal microbiota in 18 healthy participants who had received the third BNT162b. Results: The nasal S-RBD IgG level correlated significantly with plasma IgG levels until 1 month and the levels were sustained for 3 months post-vaccination. In contrast, nasal S-RBD IgA induction peaked at 1 month, albeit slightly, and correlated only with plasma IgA, but the induction level decreased markedly at 3 months post-vaccination. 16 S rRNA sequencing of the nasal microbiota post-vaccination revealed not an overall change, but a decrease in certain opportunistic bacteria, mainly Fusobacterium. The decrease in these bacteria was more pronounced in those who exhibited nasal S-RBD IgA induction, and those with higher S-RBD IgA induction had lower relative amounts of potentially pathogenic bacteria such as Pseudomonas pre-vaccination. In addition, plasma and mucosal S-RBD IgG levels correlated with decreased commensal pathogens such as Finegoldia. Conclusions: These findings suggest that the third dose of SARS-CoV-2 mRNA vaccination induced S-RBD antibodies in the nasal mucosa and may have stimulated mucosal immunity against opportunistic bacterial pathogens. This effect, albeit probably secondary, may be considered one of the benefits of mRNA vaccination. Furthermore, our data suggest that a cooperative function of mucosal and systemic immunity in the reduction of bacteria and provides a better understanding of the symbiotic relationship between the host and bacteria in the nasal mucosa. [ABSTRACT FROM AUTHOR]
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- 2023
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5. Specific mutations in H5N1 mainly impact the magnitude and velocity of the host response in mice
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Tchitchek, Nicolas, Eisfeld, Amie J, Tisoncik-Go, Jennifer, Josset, Laurence, Gralinski, Lisa E, Bécavin, Christophe, Tilton, Susan C, Webb-Robertson, Bobbie-Jo, Ferris, Martin T, Totura, Allison L, Li, Chengjun, Neumann, Gabriele, Metz, Thomas O, Smith, Richard D, Waters, Katrina M, Baric, Ralph, Kawaoka, Yoshihiro, and Katze, Michael G
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- 2013
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6. Toll-like receptor pre-stimulation protects mice against lethal infection with highly pathogenic influenza viruses.
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Shinya, Kyoko, Okamura, Tadashi, Sueta, Setsuko, Kasai, Noriyuki, Tanaka, Motoko, Ginting, Teridah E., Makino, Akiko, Eisfeld, Amie J., and Kawaoka, Yoshihiro
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INFLUENZA viruses ,RESPIRATORY infections ,PATHOGENIC microorganisms ,LABORATORY mice ,PANDEMICS - Abstract
Since the beginning of the 20th century, humans have experienced four influenza pandemics, including the devastating 1918 'Spanish influenza'. Moreover, H5N1 highly pathogenic avian influenza (HPAI) viruses are currently spreading worldwide, although they are not yet efficiently transmitted among humans. While the threat of a global pandemic involving a highly pathogenic influenza virus strain looms large, our mechanisms to address such a catastrophe remain limited. Here, we show that pre-stimulation of Toll-like receptors (TLRs) 2 and 4 increased resistance against influenza viruses known to induce high pathogenicity in animal models. Our data emphasize the complexity of the host response against different influenza viruses, and suggest that TLR agonists might be utilized to protect against lethality associated with highly pathogenic influenza virus infection in humans. [ABSTRACT FROM AUTHOR]
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- 2011
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7. A comprehensive map of the influenza A virus replication cycle.
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Matsuoka Y, Matsumae H, Katoh M, Eisfeld AJ, Neumann G, Hase T, Ghosh S, Shoemaker JE, Lopes TJ, Watanabe T, Watanabe S, Fukuyama S, Kitano H, and Kawaoka Y
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- Antiviral Agents pharmacology, Endocytosis drug effects, Host-Pathogen Interactions, Humans, Influenza A virus drug effects, Influenza A virus genetics, Influenza A virus metabolism, Internet, Protein Biosynthesis drug effects, Protein Processing, Post-Translational drug effects, Transcription, Genetic drug effects, Virus Assembly drug effects, Virus Internalization drug effects, Computational Biology, Influenza A virus physiology, Virus Replication drug effects
- Abstract
Background: Influenza is a common infectious disease caused by influenza viruses. Annual epidemics cause severe illnesses, deaths, and economic loss around the world. To better defend against influenza viral infection, it is essential to understand its mechanisms and associated host responses. Many studies have been conducted to elucidate these mechanisms, however, the overall picture remains incompletely understood. A systematic understanding of influenza viral infection in host cells is needed to facilitate the identification of influential host response mechanisms and potential drug targets., Description: We constructed a comprehensive map of the influenza A virus ('IAV') life cycle ('FluMap') by undertaking a literature-based, manual curation approach. Based on information obtained from publicly available pathway databases, updated with literature-based information and input from expert virologists and immunologists, FluMap is currently composed of 960 factors (i.e., proteins, mRNAs etc.) and 456 reactions, and is annotated with ~500 papers and curation comments. In addition to detailing the type of molecular interactions, isolate/strain specific data are also available. The FluMap was built with the pathway editor CellDesigner in standard SBML (Systems Biology Markup Language) format and visualized as an SBGN (Systems Biology Graphical Notation) diagram. It is also available as a web service (online map) based on the iPathways+ system to enable community discussion by influenza researchers. We also demonstrate computational network analyses to identify targets using the FluMap., Conclusion: The FluMap is a comprehensive pathway map that can serve as a graphically presented knowledge-base and as a platform to analyze functional interactions between IAV and host factors. Publicly available webtools will allow continuous updating to ensure the most reliable representation of the host-virus interaction network. The FluMap is available at http://www.influenza-x.org/flumap/.
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- 2013
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8. CTen: a web-based platform for identifying enriched cell types from heterogeneous microarray data.
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Shoemaker JE, Lopes TJ, Ghosh S, Matsuoka Y, Kawaoka Y, and Kitano H
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- Computational Biology, Humans, Software, Internet, Oligonucleotide Array Sequence Analysis
- Abstract
Background: Interpreting in vivo sampled microarray data is often complicated by changes in the cell population demographics. To put gene expression into its proper biological context, it is necessary to distinguish differential gene transcription from artificial gene expression induced by changes in the cellular demographics., Results: CTen (cell type enrichment) is a web-based analytical tool which uses our highly expressed, cell specific (HECS) gene database to identify enriched cell types in heterogeneous microarray data. The web interface is designed for differential expression and gene clustering studies, and the enrichment results are presented as heatmaps or downloadable text files., Conclusions: In this work, we use an independent, cell-specific gene expression data set to assess CTen's performance in accurately identifying the appropriate cell type and provide insight into the suggested level of enrichment to optimally minimize the number of false discoveries. We show that CTen, when applied to microarray data developed from infected lung tissue, can correctly identify the cell signatures of key lymphocytes in a highly heterogeneous environment and compare its performance to another popular bioinformatics tool. Furthermore, we discuss the strong implications cell type enrichment has in the design of effective microarray workflow strategies and show that, by combining CTen with gene expression clustering, we may be able to determine the relative changes in the number of key cell types.CTen is available at http://www.influenza-x.org/~jshoemaker/cten/
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- 2012
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9. Integrated network analysis reveals a novel role for the cell cycle in 2009 pandemic influenza virus-induced inflammation in macaque lungs.
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Shoemaker JE, Fukuyama S, Eisfeld AJ, Muramoto Y, Watanabe S, Watanabe T, Matsuoka Y, Kitano H, and Kawaoka Y
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- Adaptive Immunity genetics, Animals, Apoptosis genetics, Binding Sites, Caspase 1 biosynthesis, Chemotaxis genetics, Down-Regulation, Enzyme Induction genetics, Female, Glutathione Transferase genetics, Humans, Immunity, Innate genetics, Inflammation genetics, Inflammation immunology, Inflammation pathology, Inflammation virology, Lung immunology, Lung metabolism, Macaca, RNA, Messenger genetics, RNA, Messenger metabolism, Transcription Factors metabolism, Cell Cycle, Computational Biology, Influenza A Virus, H1N1 Subtype pathogenicity, Lung pathology, Lung virology, Orthomyxoviridae Infections epidemiology, Pandemics
- Abstract
Background: Annually, influenza A viruses circulate the world causing wide-spread sickness, economic loss, and death. One way to better defend against influenza virus-induced disease may be to develop novel host-based therapies, targeted at mitigating viral pathogenesis through the management of virus-dysregulated host functions. However, mechanisms that govern aberrant host responses to influenza virus infection remain incompletely understood. We previously showed that the pandemic H1N1 virus influenza A/California/04/2009 (H1N1; CA04) has enhanced pathogenicity in the lungs of cynomolgus macaques relative to a seasonal influenza virus isolate (A/Kawasaki/UTK-4/2009 (H1N1; KUTK4))., Results: Here, we used microarrays to identify host gene sequences that were highly differentially expressed (DE) in CA04-infected macaque lungs, and we employed a novel strategy - combining functional and pathway enrichment analyses, transcription factor binding site enrichment analysis and protein-protein interaction data - to create a CA04 differentially regulated host response network. This network describes enhanced viral RNA sensing, immune cell signaling and cell cycle arrest in CA04-infected lungs, and highlights a novel, putative role for the MYC-associated zinc finger (MAZ) transcription factor in regulating these processes., Conclusions: Our findings suggest that the enhanced pathology is the result of a prolonged immune response, despite successful virus clearance. Most interesting, we identify a mechanism which normally suppresses immune cell signaling and inflammation is ineffective in the pH1N1 virus infection; a dyregulatory event also associated with arthritis. This dysregulation offers several opportunities for developing strain-independent, immunomodulatory therapies to protect against future pandemics.
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- 2012
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10. Conserved host response to highly pathogenic avian influenza virus infection in human cell culture, mouse and macaque model systems.
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McDermott JE, Shankaran H, Eisfeld AJ, Belisle SE, Neuman G, Li C, McWeeney S, Sabourin C, Kawaoka Y, Katze MG, and Waters KM
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- Animals, Disease Resistance genetics, Humans, Influenza, Human immunology, Macaca, Mice, Models, Immunological, Multivariate Analysis, Systems Biology, Gene Regulatory Networks, Influenza A Virus, H5N1 Subtype pathogenicity, Influenza, Human genetics
- Abstract
Background: Understanding host response to influenza virus infection will facilitate development of better diagnoses and therapeutic interventions. Several different experimental models have been used as a proxy for human infection, including cell cultures derived from human cells, mice, and non-human primates. Each of these systems has been studied extensively in isolation, but little effort has been directed toward systematically characterizing the conservation of host response on a global level beyond known immune signaling cascades., Results: In the present study, we employed a multivariate modeling approach to characterize and compare the transcriptional regulatory networks between these three model systems after infection with a highly pathogenic avian influenza virus of the H5N1 subtype. Using this approach we identified functions and pathways that display similar behavior and/or regulation including the well-studied impact on the interferon response and the inflammasome. Our results also suggest a primary response role for airway epithelial cells in initiating hypercytokinemia, which is thought to contribute to the pathogenesis of H5N1 viruses. We further demonstrate that we can use a transcriptional regulatory model from the human cell culture data to make highly accurate predictions about the behavior of important components of the innate immune system in tissues from whole organisms., Conclusions: This is the first demonstration of a global regulatory network modeling conserved host response between in vitro and in vivo models.
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- 2011
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