Fig. 1: Immunological and virological profiling of the 2020–2021 cohort.
From: Long COVID involves activation of proinflammatory and immune exhaustion pathways
a, Symptom prevalence in individuals with LC (n = 28) and individuals who recovered (CCs, n = 24) in the 2020–2021 cohort. b, log10-transformed nAbs titers and IFNγ (ELISpot responses against the WH/2020, Delta and BA.1 variants of SARS-CoV-2) in CC (n = 9) and LC (n = 41) individuals on day 90–180 after infection. The dots are individual participants and the red bars are group medians. Samples from several time points were assessed for participants with LC. c, Quantification of SARS-CoV-2 genomic (N, E) and subgenomic (N single-guide RNA (sgRNA), E sgRNA) RNA in CCs (n = 9) and LCs (n = 41). Medians (red bars) are shown for each group. Samples from several time points were assessed for participants with LC. d, K-mean clustering across acute COVID-19 (n = 54), LCs (n = 28), CCs (n = 24) and uninfected (NC) (n = 35) individuals. All available samples were included in the k-mean analysis for the LC and CC groups. e, Heatmap of top significant (Padj < 0.05) proinflammatory genes upregulated (red) or downregulated (blue) in LCs compared to CCs or NCs at day 90–180 after SARS-CoV-2 infection. f, Transformed log2 fold change expression of the top upregulated (pink) and downregulated (dark) genes in LCs compared to CCs and NCs (Padj < 0.05).
