The immediate early gene products of human cytomegalovirus increase vascular smooth muscle cell migration, proliferation, and expression of PDGF beta-receptor.

Evidence suggests that human cytomegalovirus (HCMV) infection contributes to the development of atherosclerosis and restenosis. Because smooth muscle cell (SMC) proliferation and migration are crucial events of both processes, and because PDGF beta-receptor modulates SMC migration, we determined whether HCMV infection affects SMC proliferation, migration, and PDGF beta-receptor expression. We employed a SMC model in which HCMV infection leads to expression of only the immediate early (IE) HCMV gene products-HCMV infection of rat SMCs. We found that HCMV infection significantly (i) increased SMC proliferation (from 0.9 x 10(6) +/- 0.024 x 10(6) to 1.4 x 10(6) +/- 0.051 x 10(6) cells/well, p < 0.001); (ii) augmented SMC migration toward PDGF (from 64 +/- 37 to 116 +/- 51 cells/high power field; p < 0.01); and (iii) enhanced PDGF beta-receptor expression in a time-dependent fashion. We conclude that HCMV infection of rat SMCs increases SMC proliferation, migration, and PDGF beta-receptor expression. These findings identify further mechanisms by which CMV may contribute to the development of atherosclerosis and restenosis.