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Vascular endothelial and smooth muscle cells are unlikely to be major sites of latency of human cytomegalovirus in vivo

Heather Coleman^1,

¹ University of Cambridge, Department of Medicine, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK
² Department of Histopathology, Papworth Hospital, Cambridge, UK

Correspondence
John H. Sinclair
js{at}mole.bio.cam.ac.uk

Human cytomegalovirus (HCMV) is a frequent cause of major disease following primary infection or reactivation from latency in immunocompromised patients. It has also been suggested that there may be a link between HCMV and vascular disease. Both smooth muscle and endothelial cells are targets for primary infection with HCMV and have also been postulated as potential sites of HCMV latency. One of the most intensely studied sites of HCMV latency is the cells of the myeloid lineage; there is increasing evidence that the myeloid and endothelial lineages arise from a common precursor in the bone marrow, suggesting that endothelial cells could be another route of HCMV dissemination. However, using a highly sensitive PCR capable of detecting endogenous HCMV in myeloid cells, the HCMV genome in endothelial and smooth muscle cells isolated from the saphenous veins of seropositive patients was not detected. These data suggest that vascular endothelial and smooth muscle cells are unlikely to be important sites of HCMV latency in vivo.

Present address: University of Cambridge, Division of Virology, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK.

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