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| IJCEP Copyright © 2007-All rights reserved. |
| International Journal of Clinical and Experimental Pathology |
Int J Clin Exp Pathol 2(1),48-64;2009
Review Article
Infection and Cervical Neoplasia: Facts and Fiction
Wael I Al-Daraji and John HF Smith
Departments of Gynaecology, Department of Histopathology, Darent Valley Hospital, Dartford, Kent, UK
Received 11 March 2008; Accepted with revision 25 April 2008; Available online 28 April 2008
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.(IJCEP803003).
Key Words: Human papillomavirus (HPV), cervical neoplasia, sexually transmitted infections (STI), microbiology
Full text PDF
Address all correspondences to: Wael Al-Daraji, M.D., Histopathology Department, Darent Valley Hospital, Darenth Wood Road, Dartford
Kent, DA2 8DA, Tel: 01322 428 131, Fax 01322 428 259 (Attention Dr Wael Al-Daraji), E-mail: waldaraji@aol.com
Review Article
Infection and Cervical Neoplasia: Facts and Fiction
Wael I Al-Daraji and John HF Smith
Departments of Gynaecology, Department of Histopathology, Darent Valley Hospital, Dartford, Kent, UK
Received 11 March 2008; Accepted with revision 25 April 2008; Available online 28 April 2008
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.(IJCEP803003).
Key Words: Human papillomavirus (HPV), cervical neoplasia, sexually transmitted infections (STI), microbiology
Full text PDF
Address all correspondences to: Wael Al-Daraji, M.D., Histopathology Department, Darent Valley Hospital, Darenth Wood Road, Dartford
Kent, DA2 8DA, Tel: 01322 428 131, Fax 01322 428 259 (Attention Dr Wael Al-Daraji), E-mail: waldaraji@aol.com