Abstract
The greatest risk factor for the development of cervical and other cancers that have been linked to the human papillomavirus (HPV) family is the persistence of the virus. To persist for the decades required to develop HPV-related cancers, the virus must escape host immunity. HPV is a simple DNA virus that has evolved to escape immune attack by a combination of stealth and interference. This review focuses on the mechanisms by which HPV can evade recognition by the host immune system.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Antigen Presentation
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Antigen-Presenting Cells / physiology
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Cell Adhesion Molecules / physiology
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Cell Movement
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Chemotactic Factors / antagonists & inhibitors
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Codon
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Cytokines / antagonists & inhibitors
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Female
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Humans
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Interferons / physiology
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Papillomaviridae / genetics
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Papillomaviridae / pathogenicity*
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Papillomavirus Infections / complications
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Papillomavirus Infections / immunology*
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Signal Transduction
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T-Lymphocytes, Cytotoxic / immunology
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Uterine Cervical Neoplasms / etiology
Substances
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Cell Adhesion Molecules
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Chemotactic Factors
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Codon
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Cytokines
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Interferons