Current strategies against persistent human papillomavirus infection (Review)

Abstract

Human papillomavirus (HPV) is the most common sexually transmitted infection, exhibiting a tropism for the epidermis and mucosae. The link between persistent HPV infection and malignancies involving the anogenital tract as well as the head and neck has been well-established, and it is estimated that HPV-related cancers involving various anatomical sites account for 4.5% of all human cancers. Current prophylactic vaccines against HPV have enabled the prevention of associated malignancies. However, the sizeable population base of current infection in whom prophylactic vaccines are not applicable, certain high-risk HPV types not included in vaccines, and the vast susceptible population in developing countries who do not have access to the costly prophylactic vaccines, put forward an imperative need for effective therapies targeting persistent infection. In this article, the life cycle of HPV, the mechanisms facilitating HPV evasion of recognition and clearance by the host immune system, and the promising therapeutic strategies currently under investigation, particularly antiviral drugs and therapeutic vaccines, are reviewed.

CRISPR‐Cas system for biomedical diagnostic platforms

“…People can become infected with more than one type of HPV. In these cases, HPV16 and HPV18 account for appropriate 70% 43 . A rapid and accurate test is reported by Chen et al to detect and distinguish HPV types 16 and 18 that are carcinoma‐linked from clinical samples 44 .…”

Prevalence and genotype distribution of HPV and cervical pathological results in Sichuan Province, China: a three years surveys prior to mass HPV vaccination

“…However, the vaccines showed prominently type-restricted prophylactic efficacy. They merely induced immunity specific to certain HPV genotypes, and were unable to fend off other genotypes of the virus [4]. Studies also demonstrated that the distribution of HPV genotypes differed considerably both geographically and among populations.…”

“…HPV 6, 11, 42, 43, 44, CP8304) which were mainly found in the genital warts, and high-risk categories (e.g. HPV 16, 18, 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66 and 68),the persistent infection of which has been recognized as a strong carcinogenic factor to induce cervical cancer [ 3 , 4 ]. Because of the huge difference regarding the ability to induce cervical cancer, it was worthwhile to investigate HPV DNA genotype to improve the effect of cervical cancer screening.…”

Prevalence and genotype distribution of HPV and cervical pathological results in Sichuan Province, China: a three years surveys prior to mass HPV vaccination

“…HPV 6,11,42,43,44, CP8304) which were mainly found in the genital warts, and high-risk categories (e.g. HPV 16,18,31,33,35,39,45,51,52,53,56,58,59,66 and 68) ,the persistent infection of which has been recognized as a strong carcinogenic factor to induce cervical [3] , [4]. Because of the huge different ability to induce cervical cancer, it is meaningful to investigate HPV DNA genotype to enhancing the effect of cervical cancer screening.…”

“…However, the vaccines showed prominently type-restricted prophylactic efficacy. They merely induce immunity specific to certain HPV genotypes, and are unable to fend off other genotypes of the virus [4]. Studies also demonstrated that the distribution of HPV genotypes differs considerably both geographically and among populations.…”