Figure 3.
Molecular characteristics of the EBV-infected cells. (A) Violin plots comparing the LT-HSC signature between EBV-infected (EBV+) and uninfected (EBV−) HSCs derived from the 3 patients with CAEBV (subjects 3-5). (B) Violin plots comparing the short-term HSC (ST-HSC) signature between EBV-infected (EBV+) and uninfected (EBV−) HSCs derived from the 3 patients with CAEBV (subjects 3-5). The EBV-infected HSCs exhibited a significantly lower LT-HSC signature and a significantly higher ST-HSC signature, indicating that the infected HSCs were more active in differentiating into downstream lineages. (C) Violin plots comparing the quiescent HSC signature between EBV-infected (EBV+) and uninfected (EBV−) HSCs derived from the 3 patients with CAEBV (subjects 3-5). The EBV-infected HSCs exhibited a significantly lower quiescent HSC signature, suggesting again that the infected HSCs were more active in differentiating. (D) Violin plots comparing the signature of upregulated genes in HSC-to-MPP differentiation between EBV-infected (EBV+) and uninfected (EBV−) HSCs derived from the 3 patients with CAEBV (subjects 3-5). The infected HSCs exhibited a higher signature, indicating that the infected HSCs tended to be more primed for differentiating into MPPs. (E) Violin plots and boxplots comparing the tumor inflammation signature between PB cells derived from the 3 patients with CAEBV (subjects 3-5) vs HCs (subjects 7 and 8) (left), and EBV-infected (EBV+) vs uninfected (EBV–) PB cells derived from the 3 patients with CAEBV (subjects 3-5) (right). These results indicate that the EBV infection leads to a relatively higher level of inflammation. (F) Violin plots and boxplots comparing interferon gamma production scores between EBV-infected (EBV+) vs uninfected (EBV–) peripheral NK cells derived from the 3 patients with CAEBV (subjects 3-5). A significantly higher level of interferon gamma production was found in the infected cells. (G) Violin plots and boxplots comparing the signature of T-cell receptor signaling pathway between EBV-infected (EBV+) vs uninfected (EBV–) peripheral T cells derived from the 3 patients with CAEBV (subjects 3-5). The EBV-infected T cells exhibited a significantly higher signature of T-cell receptor signaling pathway. (H) Violin plots and boxplots comparing the T-cell exhaustion score between EBV-infected (EBV+) vs uninfected (EBV–) peripheral T cells derived from the 3 patients with CAEBV (subjects 3-5). The EBV-infected T cells had a significantly higher exhaustion score. (I) Dot plot showing the Gene Ontology (GO) terms enriched in the upregulated genes identified in EBV-infected peripheral cells compared with the uninfected cells of the 3 patients with CAEBV (subjects 3-5). T cells, NK cells, monocytes (mono), and neutrophils (neutro) were examined, and the number of differentially expressed genes were indicated at the bottom. (A-D) The black horizontal lines represent the median values, and dots in the plots represent individual cells. (E-H) In the boxplots, the box represents the interquartile range (IQR), the line within the box shows the median, and the whiskers extend up to 1.5 IQR. The signature genes used in these analyses were listed in supplemental Table 2.

Molecular characteristics of the EBV-infected cells. (A) Violin plots comparing the LT-HSC signature between EBV-infected (EBV+) and uninfected (EBV−) HSCs derived from the 3 patients with CAEBV (subjects 3-5). (B) Violin plots comparing the short-term HSC (ST-HSC) signature between EBV-infected (EBV+) and uninfected (EBV−) HSCs derived from the 3 patients with CAEBV (subjects 3-5). The EBV-infected HSCs exhibited a significantly lower LT-HSC signature and a significantly higher ST-HSC signature, indicating that the infected HSCs were more active in differentiating into downstream lineages. (C) Violin plots comparing the quiescent HSC signature between EBV-infected (EBV+) and uninfected (EBV−) HSCs derived from the 3 patients with CAEBV (subjects 3-5). The EBV-infected HSCs exhibited a significantly lower quiescent HSC signature, suggesting again that the infected HSCs were more active in differentiating. (D) Violin plots comparing the signature of upregulated genes in HSC-to-MPP differentiation between EBV-infected (EBV+) and uninfected (EBV−) HSCs derived from the 3 patients with CAEBV (subjects 3-5). The infected HSCs exhibited a higher signature, indicating that the infected HSCs tended to be more primed for differentiating into MPPs. (E) Violin plots and boxplots comparing the tumor inflammation signature between PB cells derived from the 3 patients with CAEBV (subjects 3-5) vs HCs (subjects 7 and 8) (left), and EBV-infected (EBV+) vs uninfected (EBV–) PB cells derived from the 3 patients with CAEBV (subjects 3-5) (right). These results indicate that the EBV infection leads to a relatively higher level of inflammation. (F) Violin plots and boxplots comparing interferon gamma production scores between EBV-infected (EBV+) vs uninfected (EBV–) peripheral NK cells derived from the 3 patients with CAEBV (subjects 3-5). A significantly higher level of interferon gamma production was found in the infected cells. (G) Violin plots and boxplots comparing the signature of T-cell receptor signaling pathway between EBV-infected (EBV+) vs uninfected (EBV–) peripheral T cells derived from the 3 patients with CAEBV (subjects 3-5). The EBV-infected T cells exhibited a significantly higher signature of T-cell receptor signaling pathway. (H) Violin plots and boxplots comparing the T-cell exhaustion score between EBV-infected (EBV+) vs uninfected (EBV–) peripheral T cells derived from the 3 patients with CAEBV (subjects 3-5). The EBV-infected T cells had a significantly higher exhaustion score. (I) Dot plot showing the Gene Ontology (GO) terms enriched in the upregulated genes identified in EBV-infected peripheral cells compared with the uninfected cells of the 3 patients with CAEBV (subjects 3-5). T cells, NK cells, monocytes (mono), and neutrophils (neutro) were examined, and the number of differentially expressed genes were indicated at the bottom. (A-D) The black horizontal lines represent the median values, and dots in the plots represent individual cells. (E-H) In the boxplots, the box represents the interquartile range (IQR), the line within the box shows the median, and the whiskers extend up to 1.5 IQR. The signature genes used in these analyses were listed in supplemental Table 2.

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