from Barbara Adler and Christian Sinzger writing in Cytomegaloviruses: From Molecular Pathogenesis to Intervention:
Cytomegaloviruses (CMVs) are host species-specific pathogens that cause life-long persistent infections. Under conditions of reduced immune responses CMVs can cause acute systemic infections with replication in virtually any organ. The broad organ tropism is based on an equally broad range of target cell types. Epithelial cells, fibroblasts, endothelial cells and smooth muscle cells are the major target cells that support highly productive HCMV infection. Hepatocytes, trophoblasts, neurons, macrophages and dendritic cells are also susceptible to the full replication cycle of HCMV but are apparently less productive. Granulocytes and monocytes are non-productively infected by HCMV but are assumed to contribute to hematogenous dissemination as passive vehicles. Glycoprotein complexes containing gH-gL were identified as major determinants of the cell tropism of HCMV. They are assumed to recognize entry receptors and to trigger fusion of viral and cellular membranes during entry either directly at the plasma membrane or within endosomes. Virus strains that only incorporate gH-gL-gO in their envelope have a restricted target cell range excluding endothelial cells, epithelial cells and leukocytes whereas strains that also incorporate gH-gL-pUL128-pUL130-pUL131A have an extended target cell range including these cell types. HCMV progeny of the latter strains consists of distinct populations containing either high levels or low levels of the gH-gL-pUL128-pUL130-pUL131A complex thus allowing cells to navigate virus progeny by selectively releasing or retaining virion populations that differ in their tropism.
Further reading: Cytomegaloviruses: From Molecular Pathogenesis to Intervention