Steve Bosinger

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 cell.com/cell/fulltext/…

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@MucosalGroup Thank you JoAnn!

Systems analysis reveals differential expression of endocervical genes in African women randomized to DMPA-IM, LNG implant or cu-IUD - ScienceDirect ⁦@BosingerLab⁩ #congratulations sciencedirect.com/science/articl…

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

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

10/ We would like to thank all of our wonderful collaborators and the funding sources that made this study possible.

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.

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/sc…

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.

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.