REVIEW

Postmodern cancer: the role of human immunodeficiency virus in uterine cervical cancer

B Clarke and R Chetty

Department of Anatomical Pathology, Nelson R Mandela Medical School, School of Pathology and Laboratory Medicine, Congella, 4013, Durban, Natal, South Africa

Correspondence to:
Correspondence to:
Dr B Clarke, Department of Anatomical Pathology, Nelson R Mandela Medical School, University of Natal, Private Bag 7, Congella, 4013, Durban, Natal, South Africa;
blaiseclar{at}hotmail.com

The association between cervical cancer and human papillomavirus (HPV) is well known, but its association with human immunodeficiency virus (HIV) is controversial. Coinfection with HPV and HIV is to be expected and recent epidemiological data from Africa show that cervical cancer is the most common AIDS defining neoplasm in women. Unlike other AIDS defining neoplasms, the occurrence of cervical cancer is not dependent on immune compromise. HIV alters the natural history of HPV infection, with decreased regression rates and more rapid progression to high grade and invasive lesions, which are refractory to treatment, requiring more stringent intervention and monitoring. The more aggressive behaviour is mirrored by a different molecular pathway. HIV associated cervical cancers are thought to progress through the microsatellite instability pathway, whereas HIV negative ones progress through loss of heterozygosity. Interaction is probably via viral proteins, with HIV proteins enhancing effectiveness of HPV proteins, and perhaps contributing to cell cycle disruption. Dysregulation of the cellular and humoral arms of the local and systemic immune systems may ensure disease progression. Furthermore, HPV infection may predispose to HIV infection and facilitate its progression.

Keywords: cervix cancer; human papillomavirus; human immunodeficiency virus

Abbreviations: CDC, Centres for Disease Conrol; CIN, cervical intraepithelial neoplasia; HIV, human immunodeficiency virus; HPV, human papillomavirus; IFN, interferon; IL, interleukin; LOH, loss of heterozygosity, MMR, mismatch repair; MSI, microsatellite instability; pRb, retinoblastoma protein; Th, T helper cell; TNF, tumour necrosis factor

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