The results that we present here characterize a new role for cmvIL-10 beyond its well-known function as an immune modulator during HCMV infection . The viral cytokine conferred MDA-MB-231 cells with heightened migration and invasion abilities and is likely to promote the development of breast cancer metastasis. While our studies have been conducted in vitro using cell lines, we propose an in vivo scenario in which latently infected monocyte/macrophages infiltrate the developing tumor and release cmvIL-10 (Fig. 6). Our observations that cmvIL-10 reduces expression of MTSS1, while increasing expression of uPAR, PAI-1, and MMP-3 suggest that the secreted viral cytokine can act directly on breast epithelial cells expressing IL-10R to promote reduced cell–cell adhesion and increased movement, ultimately leading to invasion into the surrounding stromal tissue and entry into bloodstream.Fig. 6Model depicting possible role of cmvIL-10 in promoting tumor metastasis. A monocyte that is latently infected with HCMV infiltrates a localized tumor, releasing cmvIL-10 that acts on tumor cells expressing the IL-10 receptor. This leads to changes in levels of MTSS1, uPAR and PAI-1, which reduce cell adhesion. Increased levels of uPAR and PAI-1 are strongly associated with increased migration and can also help activate MMP-3. Active MMP-3 degrades proteins in the extracellular matrix, facilitating access for tumor cells to invade surrounding stromal tissue and enter the bloodstream