Chlamydia pneumoniae-induced transactivation of the major immediate early promoter of cytomegalovirus: potential synergy of infectious agents in the pathogenesis of atherosclerosis.

Both cytomegalovirus (CMV) and Chlamydia pneumoniae have been associated with atherosclerosis. CMV is believed to exist in host tissues in a latent state with periodic reactivation. This study was designed to determine whether C. pneumoniae infection stimulates the expression of CMV genes. Transactivation of the CMV major immediate early promoter (MIEP) is essential for viral gene expression and viral replication. HeLa cells were transfected with a construct containing a reporter gene (chloramphenicol acetyl transferase) controlled by the MIEP. The cells were then infected with Chlamydia at 102-106 infection-forming units (IFU) per well at various times before assay of MIEP activity (72 h after transfection). Peak transactivation occurred 6 h after infection at 104 IFU. C. pneumoniae increased MIEP activity in a dose-response manner; maximal increase was >2-fold. These results suggest that if CMV and C. pneumoniae do indeed contribute to atherosclerosis, their copresence may synergistically contribute to it.