title: Cytomegalovirus and Epstein-Barr virus DNA transcription in endodontic symptomatic lesions.
abstract: OBJECTIVE
  Productive Herpesviridae infections are implicated in the etio-pathogenesis of aggressive periodontitis. However, virtually nothing is known about a possible role of herpesviruses in pulpal and periapical pathosis. This study employed a cDNA analysis to determine transcription of human cytomegalovirus (HCMV), Epstein-Barr virus (EBV) and herpes simplex virus (HSV) in 14 recalcitrant periapical lesions and in 2 periapical healthy control sites.
  
  
  METHODS
  Periapical samples were collected in conjunction with periapical surgery and kept frozen until virologic examination. RNA was isolated from periapical tissue by using a guanidinium isothiocyanate-acid phenol procedure (TRIZOL LS Reagent, GIBCO BRL, Rockville, MD). cDNAs were amplified by means of oligonucleotides targeting highly conserved regions of the test viruses and the RT-PCR-100 amplification kit (Sigma-Aldrich, St Louis, MO). Standardization of PCR primer sensitivity and validation was carried out according to established methods. Amplification products were identified by agarose gel electrophoresis.
  
  
  RESULTS
  HCMV transcript was detected in 12 of 13 symptomatic and in 1 asymptomatic periapical lesion. EBV transcript was demonstrated in 8 of the 13 symptomatic lesions but not in the asymptomatic periapical lesion. HCMV and EBV dual transcription occurred at higher frequency in periapical lesions showing radiographic bone destruction of 5 mm x 7 mm or larger than in smaller size lesions (P = 0.03; Chi-squared test). No HCMV or EBV transcription was identified in the 2 healthy control sites. HSV transcript was not detected in any study site.
  
  
  CONCLUSIONS
  The present data suggest that HCMV or EBV infections participate in the pathogenesis of periapical symptomatic lesions. Herpesviruses may produce periapical pathosis as a direct result of viral infection and replication, or as a consequence of virally induced impairment of the host defense and subsequent increased virulence of resident bacterial pathogens.
authors.affiliation: University of Southern California, School of Dentistry, Los Angeles, CA 90089, USA.
authors.forename: M
authors.initials: M
authors.lastname: Sabeti
authors.forename: Y
authors.initials: Y
authors.lastname: Valles
authors.forename: H
authors.initials: H
authors.lastname: Nowzari
authors.forename: J H
authors.initials: JH
authors.lastname: Simon
authors.forename: V
authors.initials: V
authors.lastname: Kermani-Arab
authors.forename: J
authors.initials: J
authors.lastname: Slots
mesh_terms: D000328:Adult; D000368:Aged; D001862:Bone Resorption / Q000821:virology; D016009:Chi-Square Distribution; D002648:Child; D017124:Conserved Sequence / Q000235:genetics; D003587:Cytomegalovirus / Q000235:genetics*; D003586:Cytomegalovirus Infections / Q000821:virology; D018076:DNA, Complementary / Q000235:genetics; D004279:DNA, Viral / Q000235:genetics*; D006566:Herpesviridae Infections / Q000821:virology; D004854:Herpesvirus 4, Human / Q000235:genetics*; D006801:Humans; D008875:Middle Aged; D010483:Periapical Diseases / Q000821:virology*; D010486:Periapical Tissue / Q000821:virology; D012367:RNA, Viral / Q000235:genetics; D015203:Reproducibility of Results; D018139:Simplexvirus / Q000235:genetics; D014158:Transcription, Genetic / Q000235:genetics*
chemical_list: D018076:DNA, Complementary; D004279:DNA, Viral; D012367:RNA, Viral