The immunology of genital human papilloma virus infection.
This paper reports a presentation by Margaret Stanley, Reader in Epithelial Biology, at the University of Cambridge, in which she reviews the evidence to date regarding the immunology of human papilloma virus (HPV) infection in genital warts. In this she explains that investigations into the immunology of genital wart infections indicate that the replication cycle of papilloma viruses is tightly linked to keratinocyte differentiation - a strategy for immune evasion. While the papilloma virus infects primitive basal cells, viral replication and viral assembly are confined to differentiating superficial epithelial cells. Viral replication and release are confined to cells destined for death and are not associated with inflammation. Such findings suggest that the immune system is ignorant or indifferent to the infection. Evidence from regressing genital warts in humans and animal models suggests that HPV is a cell-mediated immune response of the Th1 type offering a strategy for immunotherapy in benign disease. This is supported by evidence from trials with immunomodulatory agents. While strategies to elicit cytotoxic responses are required for malignant HPV associated lesions, the problems of immune evasion associated with these approaches should not be underestimated. Present optimal therapeutic strategies for genital human papilloma viruses infection would therefore appear to require the induction of a virus specific immune response, either by immunomodulatory agents and/or immunisation with the relevant viral antigens.
Stanley
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Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, England.
D003218:Condylomata Acuminata / Q000276:immunology*; D006801:Humans; D027383:Papillomaviridae / Q000276:immunology*; D030361:Papillomavirus Infections / Q000276:immunology*; D014412:Tumor Virus Infections / Q000276:immunology*