from Lisa P. Daley-Bauer and Edward S. Mocarski writing in Cytomegaloviruses: From Molecular Pathogenesis to Intervention:
Cytomegalovirus pathogenesis, dissemination and immunity are tied to the behaviour of myelomonocytic cells. Investigations of the roles of monocyte subsets in the dissemination of cytomegalovirus revealed that the MCMV-encoded chemokine, MCK2, controls recruitment patterns of the two major monocyte subsets (inflammatory and patrolling) to sites of infection. Monocytes give rise to both macrophages and dendritic cells that populate tissues. Mice deficient in the chemokine axis (CCR2 and CCL2 /MCP-1) do not support inflammatory monocyte emigration from bone marrow. Inflammatory monocyte-derived lineages, which are nonpermissive for MCMV, are dispensable for pathogenesis and dissemination as well as for the establishment of latency set-points. Nevertheless, recruitment of inflammatory monocytes is enhanced by elaboration of MCK2 and impairs the CTL response to delay viral clearance. In contrast, patrolling monocytes support MCMV replication and contribute to dissemination patterns in the host. Studies in CX3CR1-deficient infected mice show reduced viral dissemination to salivary glands, consistent with the reduced survival of patrolling monocytes in these animals. HCMV studies suggest myelomonocytic progenitor cells, including inflammatory and patrolling monocyte subsets, are associated with acute as well as latent infections. MCMV latency in mice occurs in myeloid as well as epithelial and endothelial cell lineages. In this paper, we review the current understanding of myelomonocytic lineage cells in the establishment of cytomegalovirus infections based on human and murine studies.
Further reading: Cytomegaloviruses: From Molecular Pathogenesis to Intervention