Interaction of human cytomegalovirus with p53: possible role in coronary restenosis.

E. Speir, E. S. Huang, R. Modali, M. B. Leon, F. Shawl, T. Finkel, S. E. Epstein

Research output: Contribution to journalArticlepeer-review


Restenosis occurs in 25-50% of patients. Within 1-6 months after coronary angioplasty, excessive injury-induced smooth muscle cell (SMC) proliferation contributes to the development of restenosis; its causes remain unknown. The results of this study implicate human cytomegalovirus (HCMV) and HCMV-induced abnormalities in p53 function in the restenosis process. Almost 40% of restenosis lesions, obtained by atherectomy, demonstrated increased SMC p53 levels by p53 immunopositivity; sequencing revealed the p53 to be the wild type. A strong correlation was found between p53 immunopositivity and the presence of HCMV DNA. Moreover, the HCMV IE84 protein co-immunoprecipitates with p53, and p53 transcriptional capacity is reduced by IE84. Thus, HCMV may play a causal role in restenosis, which may be at least partly mediated by inhibiting p53 suppressor effects.

Original languageEnglish (US)
Pages (from-to)78-81
Number of pages4
JournalScandinavian Journal of Infectious Diseases, Supplement
StatePublished - 1995
Externally publishedYes

ASJC Scopus subject areas

  • Microbiology (medical)
  • Immunology


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