Project 1: pediatric COVID-19: Nehar-Belaid et al Nature Communications, 2025
💡 We applied a multidimensional approach to decipher the immune responses to SARS-CoV-2 infection in 2-month-old hospitalized infants. We analyzed: (i) single cell RNA-seq from PBMCs, (ii) serum cytokines and (iii) antibody responses.
💡 We also compared our findings to children and adult cohorts. Infants displayed a similar ISG signature in monocytes but a markedly enhanced ISG signature in T and B cells, which is consistent with infant specific immune features.
👉 This study was published in Nature Communications in 2025.
Project 2: Epigenetic memory of COVID-19 in young adults: Cheong et al Cell, 2023
Epigenetic Memory of COVID-19 in Innate Immune Cells and Their Progenitors.
Collboration with Josefowicz (Weill Cornell Medicine) and Ucar (The Jackson laboratory) labs
This project was published in Cell in 2023
Highlights:
1- Severe COVID-19 programs durable epigenetic changes and hyper-activation in monocytes
2- Circulating HSPC capture post-COVID-19 changes in hematopoiesis and stem cell programs
3- Post-COVID-19 HSPC convey epigenetic and transcriptional memory to mature progeny cells
4- IL-6 contributes to epigenetic reprogramming of mouse and human HSPC and myeloid cells
Summary:
Inflammation can trigger lasting phenotypes in immune and non-immune cells. Whether and how human infections and associated inflammation can form innate immune memory in hematopoietic stem and progenitor cells (HSPC) has remained unclear. We found that circulating HSPC, enriched from peripheral blood, captured the diversity of bone marrow HSPC, enabling investigation of their epigenomic reprogramming following coronavirus disease 2019 (COVID-19). Alterations in innate immune phenotypes and epigenetic programs of HSPC persisted for months to 1 year following severe COVID-19 and were associated with distinct transcription factor (TF) activities, altered regulation of inflammatory programs, and durable increases in myelopoiesis. HSPC epigenomic alterations were conveyed, through differentiation, to progeny innate immune cells. Early activity of IL-6 contributed to these persistent phenotypes in human COVID-19 and a mouse coronavirus infection model. Epigenetic reprogramming of HSPC may underlie altered immune function following infection and be broadly relevant, especially for millions of COVID-19 survivors.