PapillomavirusA resource for Papillomavirus Immunobiology.
Edited by: Kevin Gaston"invaluable for its multiple perspectives and concise summary of a large body of research" (MedicalScienceBooks.com); "a good reference and review" (Doodys); "a very valuable reference" (Microbiol. Today) read more ...
Leading scientists from around the world review current hot-topics on small DNA tumour virus research providing a fascinating overview of their molecular biology and interactions with the host.
(adapted from Margaret A Stanley in Papillomavirus)
Papillomavirus Immunobiology: Papillomaviruses are ubiquitous and successful infectious agents that are characterised by absolute species specificity and tissue tropism. The infectious cycle of these viruses is tailored to the differentiation programme of the target cell - the keratinocyte - different phases of permissive viral growth accompanying the steady maturation of the keratinocyte as it progresses up the epithelium to its destiny as a terminally differentiated squame. This infectious cycle raises several important issues with respect to immune recognition. Firstly infection and vegetative viral growth are absolutely dependent upon a complete programme of keratinocyte differentiation. Virus infects primitive basal keratinocytes, probably targeting stem cells, but high level viral expression of viral proteins and viral assembly occur only in the upper layers of the stratum spinosum and granulosum of squamous epithelia. Viral gene expression is confined to the keratinocyte and there is no evidence from clinical infections that viral genes are expressed in any cell other than keratinocytes or cells with the potential for squamous maturation. Secondly the replication cycle takes a long time, even in the best scenario the time from infection to release of virus will take about 3 weeks since this is the time taken for the basal keratinocyte to undergo complete differentiation and desquamate. In reality the period between infection and the appearance of lesions is highly variable and can vary from weeks to months indicating that the virus can effectively evade the immune system. Thirdly there is no cytolysis or cytopathic death as a consequence of viral replication and assembly. These key events for the virus occur in the differentiating keratinocyte, a cell destined for death and desquamation far from the sites of immune activity. The virus actually delays nuclear condensation in differentiating keratinocytes forming the koilocyte, the pathognomic cell of HPV infection. This may be the consequence (at least in high risk HPV infections) of the combined effects of viral E6 and E7 proteins in halting apoptosis until viral replication is completed but then the virus laden keratinocyte proceeds to its inevitable fate, death by natural causes. As a consequence of this, HPV infection is not accompanied by inflammation, there is no obvious "danger signal" to alert the immune system. This is a viral strategy that results in persistent, chronic infections as the host remains ignorant of the pathogen for long periods. The central questions therefore are, does natural infection with HPV evoke a host response, what is the nature of this response, when and how does it occur, what is the role of humoral and cell mediated immunity in the natural history of genital HPV associated disease and how do virus positive neoplasms arise in the face of host defences? This review discusses the cell mediated immune response to HPV infection. An authoritative reference on Papillomavirus is provided by the new book Papillomavirus.
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