Fig. 1: HSCs, committed progenitor cell populations in the BM, are altered upon chronic LCMV CL13 infection.

a Gating strategies for identifying different populations in the BM by surface marker expression: LSK cells (Lin⁻, Sca-1⁺, c-kit⁺), LK cells (Lin⁻, Sca-1⁻, c-kit⁺), LT HSCs (Lin⁻, Sca-1⁺, c-kit⁺, CD135⁻, CD34⁻), ST HSCs (Lin⁻, Sca-1⁺, c-kit⁺, CD135⁻, CD34⁺), MEPs (Lin⁻, Sca-1⁻, c-kit⁺, CD16/32^low, CD34⁻), GMPs (Lin⁻, Sca-1⁻, c-kit⁺, CD16/32^high, CD34⁺), CMPs (Lin⁻, Sca-1⁻, c-kit⁺, CD16/32^low, CD34⁺), CLPs (Lin⁻, c-kit^low, CD135⁺, CD127⁺), and CDPs (Lin⁻, Sca-1⁻, c-kit^low, CD135/CD115⁺, CD127⁻). b Each HSC and progenitor population in the BM of uninfected or LCMV-infected mice (10 or 30 days postinfection) was identified by gating on surface markers. c The frequency of each HSC and progenitor cell in the lineage marker-negative populations between the uninfected and LCMV-infected groups is summarized in a bar plot. Graphs for 10 days post-LCMV infection (early chronic phase) and 30 days post-LCMV infection (late chronic phase) are presented. d The absolute numbers of HSCs and progenitor cells in two million live BM cells were analyzed. e tSNE visualization of HSC and progenitor cell populations in the BM. Each population was visualized at distinct locations on the tSNE map, and clustering was applied with the Barnes-Hut implementation algorithm using the following parameter: perplexity = 30. The bar graphs show the means ± SDs (5 mice in each group). Each experiment was repeated 3 times. The p values in the figures indicate the following: *P < 0.05; **P < 0.01; **P < 0.01; ***P < 0.001.