Single-cell signatures of EBV immune scarring in B-cells [MANUSCRIPT - Submitted to iScience]

CORRECTION / LIMITATIONS NOTICE (June 2026): The author flags serious limitations that undermine the central claim of this manuscript. The conclusions about EBV-induced "immune scarring" in B cells and the drug classes said to reverse it should be treated as unsupported. The data and code remain available for transparency. This manuscript was not accepted for publication. It is a standalone research paper and is not a companion to, and does not affect, any patent filing. 1. Small foundation. The core analysis rests on a 19-cell basis, far too few cells to support the conclusions drawn.2. EBV was never measured. No EBV status or viral signal was measured in the dataset; the "EBV" framing is inferred, not observed.3. Circular phenotype definition. The "scarring" score was defined from curated gene sets; the cluster scoring highest on that score was then labeled the "scarred" state, and that label was used to justify the analysis. There is no external or clinical anchor for "scarring."4. Mixed tissue. B cells were not subset to a single tissue; blood and skin cells were combined. The notice reflects responsible self-correction made on the author's own review. --- ORIGINAL DESCRIPTION (conclusions UNSUPPORTED, preserved for the record) --- This manuscript presents single-cell transcriptomic analysis of EBV-induced immune scarring in B cells. Submission version for iScience (Cell Press), February 2026. The study integrates virology, immunology, and computational biology to demonstrate that Epstein-Barr virus creates durable transcriptional "immune scarring" in B cells. Using scVI and LINCS L1000, we identify drug classes (JAK inhibitors, HDAC inhibitors) that reverse these states. Part of research program on EBV-scleroderma connections. Related: https://doi.org/10.5281/zenodo.18227328 (code/data) Files: Main manuscript PDF + 4 supplementary figures + 7 supplementary tables