Multiple aspects of human papillomavirus infections

Abstract

Human Papillomavirus (HPV) types are thought to have originated very early during human evolution and are now defined by their genomic sequence (late, L1), differing by >10% among them. Importantly, viral types are cell-type specific and usually produce different kinds of lesions, benign or malignant. In addition, these types have co-evolved with their hosts and have generated what we call now intratype variants. Variants of HPV types are found associated with the ethnicity of the populations and have been grouped geographically. It is believed that HPV intratype variants may differ in biological behavior. Recognition of the crucial role that some specific HPV types play in cervical cancer development is highly important for their prevention and implementation of public health strategies to control cervical cancer, still the leading cause of death among cancer patients in many developing nations as reported by Lizano et al. (Arch Med Res 40:428-434, 2009). The role of these virus infections has been established: (1) by the regular presence of HPV deoxyribonucleic acid (DNA) in the respective tumor biopsy specimens, (2) by the demonstration of viral oncogene expression (early, E6 and E7) in tumor material, (3) by the identification of transforming properties of these genes, (4) by the requirement for E6 and E7 expression for maintaining the malignant phenotype of cervical carcinoma cell lines, (5) by the interaction of viral oncoproteins with growth-regulating host-cell proteins, and (6) by epidemiologic studies pointing to these HPV infections as the major risk factor for cervical cancer development. Modifications in host-cell genes, most likely engaged in the control of HPV gene expression in proliferating cells, emerge as important events in HPV-mediated carcinogenesis as reported by zur Hausen (J Natl Cancer Inst 92:690-698, 2000).