Associate Professor at Emory University. Immunologist; Systems Biologist; Using genomics to study viral infections.

Joined March 2017
35 Photos and videos
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20 Sep 2023
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: bit.ly/CFARWorkshopFall23
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Our new work with @PaiardiniLab and @elise_viox by @amitupadhyay85 featured by @SciImmunology
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. scim.ag/3zF
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Steve Bosinger retweeted
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. scim.ag/3zF
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Steve Bosinger retweeted
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: scim.ag/3yf
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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/doi/10.1126/scii…
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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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10/ We would like to thank all of our wonderful collaborators and the funding sources that made this study possible.
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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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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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