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. Transacti...

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Bibliographic Details
Published in:The Journal of infectious diseases 2000-02, Vol.181 (2), p.787-790
Main Authors: Wanishsawad, Chad, Zhou, Yi Fu, Epstein, Stephen E.
Format: Article
Language:English
Subjects:
Antigens, Viral - genetics
Antigens, Viral - metabolism
Arteriosclerosis - virology
Atherosclerosis
Atherosclerosis (general aspects, experimental research)
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Cell lines
Chlamydia pneumoniae
Chlamydophila pneumoniae
Chlamydophila pneumoniae - physiology
Chloramphenicol O-Acetyltransferase - genetics
Chloramphenicol O-Acetyltransferase - metabolism
Concise Communications
Cytomegalovirus
Cytomegalovirus - genetics
Gene Expression Regulation, Viral
HeLa Cells
Humans
Immediate-Early Proteins - genetics
Immediate-Early Proteins - metabolism
Infections
major immediate early promoter
Medical sciences
Pathogens
Plasmids
Plasmids - genetics
Promoter Regions, Genetic - genetics
Transcriptional Activation
Transfection
Virus Activation
Virus Replication
Viruses
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Description
Summary: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 trans-activation 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.
ISSN:0022-1899
1537-6613
DOI:10.1086/315235