Mechanisms used by human papillomaviruses to escape the host immune response.
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.
Kanodia
Shreya
S
Department of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90033, USA.
Fahey
Laura M
LM
Kast
W Martin
WM
D017951:Antigen Presentation; D000938:Antigen-Presenting Cells / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000502:physiology; D002465:Cell Movement; D002630:Chemotactic Factors / Q000037:antagonists & inhibitors; D003062:Codon; D016207:Cytokines / Q000037:antagonists & inhibitors; D005260:Female; D006801:Humans; D007372:Interferons / Q000502:physiology; D027383:Papillomaviridae / Q000235:genetics / Q000472:pathogenicity*; D030361:Papillomavirus Infections / Q000150:complications / Q000276:immunology*; D015398:Signal Transduction; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D002583:Uterine Cervical Neoplasms / Q000209:etiology
D015815:Cell Adhesion Molecules; D002630:Chemotactic Factors; D003062:Codon; D016207:Cytokines; D007372:Interferons