CD4 and Epstein-Barr virus infection: This finding aligned with the literature-proposed hypothesis that EBV infection may promote Bartonella henselae dissemination through transient immunosuppression, whereby acute EBV infection activated CD4+/CD8+ T cells and natural killer (NK) cells to control EBV replication and thereby temporarily impaired immune responses against other pathogens (e.g., Bartonella) (8).