TNF and infection: Since a proinflammatory state provides the tools to drive infected monocytes from the blood into the tissue to promote viral dissemination during the early infection stage, HCMV induces infected monocytes to display a unique M1-like/M2-like polarization signature that is skewed toward the classical M1-like activation phenotype [65] and increases secretion of proinflammatory cytokines and chemokines, including IL-1β, IL-6, and TNF-α [66].