Research Paper Volume 15, Issue 17 pp 8976—8992
Herpesvirus latent infection promotes stroke via activating the OTUD1/NF-κB signaling pathway
Figure 6. Key gene selection for herpesvirus latency-mediated stroke occurrence. (A) Venn diagram of the intersection of important module genes identified by WGCNA and differentially expressed genes from wild-type and mutant herpesvirus infection. (B) ROC curve analysis of the expression of OTUD1, NFIL3, and OSM genes in relation to stroke disease occurrence. Con (n = 20) represents the control group samples, and IS (n = 20) represents the stroke group samples. (C) Boxplots of differential expression of OTUD1 in brain tissue infected with wild-type and mutant herpesvirus. MOCK (n = 3) represents mock-infected brain tissue samples, MHV-68 (n = 3) represents wild-type herpesvirus-infected brain tissue samples, and ORF73 (n = 3) represents mutant herpesvirus-infected brain tissue samples.