Format

Send to

Choose Destination
Int J Clin Exp Pathol. 2009;2(1):48-64. Epub 2008 Apr 28.

Infection and cervical neoplasia: facts and fiction.

Author information

1
Department of Pathology, University of Nottingham Nottingham, UK. waldaraji@aol.com

Abstract

Whilst there is strong evidence that human papillomavirus (HPV) is the principal aetiological agent in cervical neoplasia, some other sexually transmitted agents may either contribute or protect against cervical carcinogenesis, such as the herpes virus family (HSV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), human immunodeficiency virus (HIV) or Chlamydia trachomatis (CT). Epidemiological studies suggest that HSV may have a role in cervical neoplasia, but there is no clear supportive experimental evidence. Serological studies have also failed to reveal a difference in the prevalence of antibodies to CMV and EBV between patients with cervical cancer and controls. However, longitudinal seroepidemiological studies have provided evidence that CT is an independent risk factor for the development of cervical squamous carcinoma and this association is serotype specific. The increased risk of cervical neoplasia in patients infected with HIV has been recognised for over a decade and HIV may interact with HPV either by alternating HPV gene transcription or by immunosuppression. Finally extensive experimental and limited epidemiological evidence suggests that adeno-associated viruses (AAV) may have antioncogenic activity in man and may protect against the development of cervical cancer. At present the mechanism of this action is unclear but may relate to AAV-induced regulation of HPV gene expression and the HPV life cycle. In this review we summarize the current literature relating to the associations and mechanisms of cervical carcinogenesis by each of these infectious microorganisms.

KEYWORDS:

Human papillomavirus (HPV); cervical neoplasia; microbiology; sexually transmitted infections (STI)

PMID:
18830380
PMCID:
PMC2491386

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center