Steve Bosinger
@BosingerLab
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Associate Professor at Emory University. Immunologist; Systems Biologist; Using genomics to study viral infections.
Atlanta, GA
Joined March 2017
Deep analysis of infant #immune responses to #SARSCoV2 (omicron) #proteomics #multiomics From team including our collaborators: @SetteLab @Alba_Grifoni @YupengFeng @BosingerLab @purveshkhatri Bali Pulendran, and others. @CellCellPress
https://t.co/c0NQqTxpSN
cell.com
Multi-omics analysis of blood and nasal samples from human infants and their mothers indicates strong and sustained immunity following SARS-CoV-2 infection during the initial months of life.
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Join us for a new course offering this October. Registration is limited so be sure to sign up soon.
Are you a faculty member, postdoctoral fellow, or graduate student actively engaged in research & looking to master single-cell RNA-Seq data analysis? Attend a new #EmoryCFAR Systems Immunology Core-hosted 8-week course detailed below. Apply here by 9/25: https://t.co/3EtNfDj9di
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New primate research by @elise_viox and colleagues from @BosingerLab and @PaiardiniLab corroborates the theory that too little IFN-I exacerbates viral infection, while too much IFN-I leads to harmful immune hyperactivation. https://t.co/O4dH2AKvkR
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New primate research by @elise_viox and colleagues from @BosingerLab and @PaiardiniLab corroborates the theory that too little IFN-I exacerbates viral infection, while too much IFN-I leads to harmful immune hyperactivation. https://t.co/O4dH2AKvkR
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A new study in animals evaluates how the presence of anti-viral interferon-I (IFN-I) and related signaling affects #SARSCoV2 outcomes. @elise_viox @BosingerLab @PaiardiniLab Learn more: https://t.co/QMRaGCQaGh
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10/ We would like to thank all of our wonderful collaborators and the funding sources that made this study possible.
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9/ We would like to dedicate this study in loving memory of our friend & colleague Timothy Hoang. He made crucial contributions to the fields of HIV cure & SARS-CoV-2 research during his short but impactful career & is remembered for his drive, intelligence, and love of science.
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8/ Based on these results, we conclude that although IFN-I is beneficial in controlling SARS-CoV2 replication, excessive uncontrolled inflammation driven by IFN-I-signaling plays an important role in SARS-CoV2 pathogenesis.
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7/ scRNA-Seq showed that IFNmod treatment inhibited accumulation of CD163+MRC1- macrophages & reduced the expression of inflammatory mediators in this subset in BAL. Downregulation of genes related to inflammasome activation, stress response, and cell death was observed in lungs.
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6/ Bulk RNA-Seq profiling of BAL, PBMC, and whole blood showed that ISG expression was downregulated in IFNmod-treated RMs along with a potent attenuation of systemic inflammation and inflammasome activation in lower airways.
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5/ In vivo, IFNmod treatment resulted in a 1-3 log-fold reduction in viral load in the airways of SARS-Cov2 infected RMs.
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4/ In vitro, IFNmod inhibited SARS-CoV2 infection in Calu-3 cells with similar efficacy to IFNα and Nirmatrelvir when treatment was initiated before infection.
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3/ Treatment of uninfected RMs with IFNmod resulted in a modest upregulation of antiviral IFN-stimulated genes (ISGs); while the inflammatory genes remained unchanged.
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2/ We used a mutated IFNα2 (IFNmod) to study the effect of modulating IFN-I on viral replication and pathogenesis in SARS-CoV2 infected rhesus-macaques (RMs).
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1/ Absolutely thrilled to announce the publication of our research on modulation of type I interferon in rhesus macaques! Our work was accomplished through close collaboration with the @PaiardiniLab and has now been featured in @SciImmunology.
science.org
Administration of a mutated IFN-α2 to rhesus macaques limited viral replication and pathogenesis during SARS-CoV-2 infection.
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Based on these results, we conclude that although IFN-I is beneficial in controlling SARS-CoV2 replication, excessive uncontrolled inflammation driven by IFN-I-signaling plays an important role in SARS-CoV2 pathogenesis.
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scRNA-Seq showed that IFNmod treatment inhibited accumulation of CD163+MRC1- macrophages & reduced the expression of inflammatory mediators in this subset in BAL. Downregulation of genes related to inflammasome activation, stress response, and cell death was observed in lungs.
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Bulk RNA-Seq profiling of BAL, PBMC, and whole blood showed that ISG expression was downregulated in IFNmod-treated RMs along with a potent attenuation of systemic inflammation and inflammasome activation in lower airways.
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In vivo, IFNmod treatment resulted in a 1-3 log-fold reduction in viral load in the airways of SARS-Cov2 infected RMs.
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In vitro, IFNmod inhibited SARS-CoV2 infection in Calu-3 cells with similar efficacy to IFNα and Nirmatrelvir when treatment was initiated before infection.
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