Human Papillomavirus Infections of the Lower Genital Tract

Dear Colleagues,

Human papillomavirus (HPV) is the most common sexually transmitted agent. The biology of the virus and its link with malignancies is well established, with cancers involving the anogenital (cervical, vaginal, vulvar, penile, anal) tract as well as the head and neck.

HPV is a small deoxyribonucleic acid (DNA) virus of approximately 7900 base pairs. DNA sequencing techniques have enabled HPV typing and characterization, with each type defined as distinct by having less than 90% DNA base-pair homology with any another HPV type. There are over 40 HPV types that infect the anogenital area.

The HPV genome encodes DNA sequences for six early (E) proteins that regulate viral genes and cell transformation, two late (L) proteins that form the shell of the virus, and a region of regulatory DNA sequences.

The two HPV proteins that are involved in the development of malignant disease are E6 and E7. Both E6 and E7 proteins are expressed in HPV-associated anogenital malignant tumors, where they neutralize two intracellular proteins, namely p53 and retinoblastoma protein, leading to epithelial cell immortalization.

Progression to the malignant phenotype probably involves a genetic change in the pathways controlling intracellular or intercellular signaling as well as chromosomal instability.

Three different vaccines, which vary in the number of HPV types they contain and target, have been clinically developed: a quadrivalent HPV vaccine targets HPV types 6, 11, 16, and 18. A 9-valent vaccine targets the same HPV types as the quadrivalent vaccine as well as types 31, 33, 45, 52, and 58. A bivalent vaccine (Cervarix) targets HPV types 16 and 18.

These prophylactic vaccines contain inactive HPV L1 VLPs triggering neutralizing antibodies against HPV types when they are administered. They elicit a strong humoral immune response to protect against the diseases and pre-neoplastic lesions caused by HPV.

The aim of this Special Issue is to provide insights into the mechanism of development of HPV-associated benign and malignant lesions. For this purpose, I invite you to submit research articles, review articles, and short communications related to HPV, such as virus–host interactions, signaling pathways, immune evasion, epigenomics, clinical studies, and therapeutics. As a Guest Editor of this Special Issue, I look forward to reviewing your submissions and, together, defining the present state of the science.

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