Molecular Mechanism and Potential Targets for Blocking HPV-Induced Lesion Development
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A Comparative Approach to Characterize the Landscape of Host-Pathogen Protein-Protein Interactions
Published on: July 18, 2013
E Guzmán-Olea1, V H Bermúdez-Morales, O Peralta-Zaragoza
1Division of Chronic Infections and Cancer, Research Center for Infectious Diseases, Instituto Nacional de Salud Pública, Avenida Universidad No. 655, Cuernavaca 62100, Morelos, Mexico.
Abstract:
Persistent infection with high-risk HPV is the etiologic agent associated with the development of cervical cancer (CC) development. However, environmental, social, epidemiological, genetic, and host factors may have a joint influence on the risk of disease progression. Cervical lesions caused by HPV infection can be removed naturally by the host immune response and only a small percentage may progress to cancer; thus, the immune response is essential for the control of precursor lesions and CC. We present a review of recent research on the molecular mechanisms that allow HPV-infected cells to evade immune surveillance and potential targets of molecular therapy to inhibit tumor immune escape.
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