A subset of patients who have undergone coronary angioplasty develop r
estenosis, a vessel renarrowing characterized by excessive proliferati
on of smooth muscle cells (SMCs). Of 60 human restenosis lesions exami
ned, 23 (38 percent) were found to have accumulated high amounts of th
e tumor suppressor protein p53, and this correlated with the presence
of human cytomegalovirus (HCMV) in the lesions. SMCs grown from the le
sions expressed HCMV protein IE84 and high amounts of p53. HCMV infect
ion of cultured SMCs enhanced p53 accumulation, which correlated tempo
rally with IE84 expression. IE84 also bound to p53 and abolished its a
bility to transcriptionally activate a reporter gene. Thus, HCMV, and
IE84-mediated inhibition of p53 function, may contribute to the develo
pment of restenosis.