In their discussion, the authors highlighted the potential for CPXV-mediated upregulation of IL-6 as beneficial to systematic spread as CPXV may use IL-6-attracted macrophages and monocytes to disseminate within the host [197,204], though severe tissue damage resulting from the cytopathic effects of CPXV infection could be the cause of increased IL-6 levels in more virulent infections as damaged and dying cells release IL-6 [205,206]. This evidence concerns the gene IL6 and infection.