| IJCEP Copyright © 2007-All rights reserved. |
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 correspondence 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 correspondence 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
 | |  | |  | |  | |  | |  |
