Summary
While high‐risk human papillomavirus (HR‐HPV) infection is related to the development of cervical, vulvar, anal, penile and oropharyngeal cancer, low‐risk human papillomavirus (LR‐HPV) ...infection is implicated in about 90% of genital warts, which rarely progress to cancer. The carcinogenic role of HR‐HPV is due to the overexpression of HPV E5, E6 and E7 oncoproteins which target and modify cellular proteins implicated in cell proliferation, apoptosis and immortalization. LR‐HPV proteins also target and modify some of these processes; however, their oncogenic potential is lower than that of HR‐HPV. HR‐HPVs have substantial differences with LR‐HPVs such as viral integration into the cell genome, induction of p53 and retinoblastoma protein degradation, alternative splicing in HR‐HPV E6‐E7 open reading frames, among others. In addition, LR‐HPV can activate the autophagy process in infected cells while HR‐HPV infection deactivates it. However, in cancer HR‐HPV might reactivate autophagy in advance stages. Autophagy is a catabolic process that maintains cell homoeostasis by lysosomal degradation and recycling of damaged macromolecules and organelles; nevertheless, depending upon cellular context autophagy may also induce cell death. Therefore, autophagy can contribute either as a promotor or as a suppressor of tumours. In this review, we focus on the role of HR‐HPV and LR‐HPV in autophagy during viral infection and cancer development. Additionally, we review key regulatory molecules such as microRNAs in HPV present during autophagy, and we emphasize the potential use of cancer treatments associated with autophagy in HPV‐related cancers.
Human papillomavirus (HPV) is closely linked with the pathogenesis of cervical cancer and many other cancers. HPV vaccines are vaccines that prevent infection from certain types of human ...papillomavirus. However, despite the various prevention strategies and treatments, such as HPV screening, prophylactic HPV vaccines, surgery, radiotherapy, and chemotherapy, the disease burden remains heavy worldwide. Currently, three types of prophylactic vaccines—quadrivalent HPV vaccines, bivalent HPV vaccines, and a new nonavalent HPV vaccine—are commercially available. Although these vaccines protect against 90% of HPV infections, their capacity to eliminate pre-existing infections is limited. In this Topical Collection, we aim to systematically cover the progress, current status, and future prospects of various vaccines being developed for the prevention and treatment of HPV-associated lesions and cancers.
Abstract The oncogenic potential of papillomaviruses (PVs) has been appreciated since the 1930s yet the mechanisms of virally-mediated cellular transformation are still being revealed. Reasons for ...this include: a) the oncoproteins are multifunctional, b) there is an ever-growing list of cellular interacting proteins, c) more than one cellular protein may bind to a given region of the oncoprotein, and d) there is only limited information on the proteins encoded by the corresponding non-oncogenic PVs. The perspective of this review will be to contrast the activities of the viral E6 and E7 proteins encoded by the oncogenic human PVs (termed high-risk HPVs) to those encoded by their non-oncogenic counterparts (termed low-risk HPVs) in an attempt to sort out viral life cycle-related functions from oncogenic functions. The review will emphasize lessons learned from the cell culture studies of the HPVs causing mucosal/genital tract cancers.
Globally, 4.5% of cancers are due to the human papillomavirus (HPV). In the United States, 80 million people are infected with HPV, and the incidence of HPV oropharyngeal cancer has surpassed HPV ...cervical cancer. The highest burden of oropharyngeal cancer is seen in middle‐aged and increasingly older White men. HPV vaccination promises to change the epidemiology of this disease, but HPV vaccination rates remain too low today to reduce disease transmission.
Squamous cell carcinoma accounts for 95% of head and neck cancers (HNSCC). Recently, Human papilloma virus associated HNSCC have shown rising incidence rates specifically caused by HPV-16 subtype. ...There have been limited data to differentiate the pathological and prognostic behaviors of HPV+ versus HPV- HNSCC. So, that is the aim of our study.
Data of 8802 HNSCC patients were extracted from the Surveillance, Epidemiological, and End Results (SEER) database diagnosed from 2000-2020. The histopathological classification of HPV+ and HPV-HNSCC were according to WHO ICD-0-3 classification. Cox regression hazard model was performed using SPSS 25 to assess age, race, sex, radiotherapy, chemotherapy and surgery as predictors for outcome.
HPV+ and HPV- HNSCC were found to be more common in males and white race. Increasing age was associated with poorer prognosis in HPV+ with a hazard ratio (HR) of 1.05; P<0.05, however it was insignificant predictor for HPV-; P>0.05. Surgery, radiotherapy and chemotherapy were all associated with better outcomes for HPV+; HR: 0.21, 0.23, 0.83; respectively; P<0.05. For HPV-, having surgery and radiotherapy were significant good prognostic factors; HR: 0.35 and 0.28 respectively; P<0.05. while chemotherapy wasn't significant; P>0.05. Race and Sex weren't statistically significant for HPV+ and HPV-HNSCC.
HPV+ HNSCC Showed an overall better prognosis than HPV- HNSCC. In terms of demographic characteristics. Increasing age had a poor prognostic outcome for HPV+ but no impact on prognosis for HPV-. Age and Sex were insignificant predictors for both groups. Surgery and Radiotherapy showed better prognostic value for both groups. Our results showed better outcomes of surgery and radiotherapy in HPV+ HNSCC compared to HPV- HNSCC. Chemotherapy showed slightly good prognostic outcomes for HPV+ but had no impact on outcomes for HPV-. We recommend radiotherapy and surgery to be the first line of treatment for both HPV+ and HPV- HNSCC. Chemotherapy can be preserved for selective HPV+ patients while for HPV- it had no value so, we don't recommend and we can avoid unnecessary side effects unless there are other indications.
Background
Cervical cancer (CC) is the fourth most common malignancy of the female genital tract. Human Papillomavirus (HPV) is the main cause of precancerous lesions and CC cases worldwide
Objective
...We assessed the prevalence and distribution of HPV types and their association with precancerous lesions and CC.
Methods
HPV genotypes were detected by 3 methods depending on the year of in which the sample was analyzed: MY09/11 RFLPs (1997 to 2010), GP5+/6+ primer systems (2005 to 2010) and INNO-LiPA HPV Genotyping Extra (2010 to 2019) in cervical samples (No-IL: 4445; LSIL: 2464; HSILs: 151 and CC: 253) from women from southern Mexico.
Results
The overall HPV prevalence was 54.17%, and hpv-16 was the most common genotype. In single infection, the high-risk HPV genotypes (group 1) were associated with squamous intraepitelial lesions (LSIL: HPV–39 (OR = 10.58, 95% CI 4.09–27.36, P < .001); HSIL: HPV-31 (OR = 14.76, 95% CI 6.56–33.20, P < .001); and CC: HPV-16 (OR = 25.01, 95% CI 18.83–33.21, P < .001). In multiple infections, the HPV genotypes (HPV-16 and HPV-18) were also associated with a high risk of lesions LSIL: HPV-18 (OR = 3.45; 95% CI 1.36–8.91; P = .009); HSIL: HPV-18 (OR = 5.12; 95% CI 1.21–21.68; P = .026); and CC: HPV-16 (OR = 3.03; 95% CI 1.72–5.32; P < .001) compared to single infection. In the analysis adjusted for age, giving birth, and cigarette smoking, a significant increase in the risk of LSIL, HSIL, and CC was maintained.
Conclusions
This study provides current data on the prevalence and distribution of HPV genotypes in women from southern Mexico, which could serve as a valuable reference to guide nationwide CC screening programs and provide scientific evidence that could be useful for vaccine development efforts. Likewise, it was identified that infection with carcinogenic HPV genotypes is an independent risk factor for LSIL, HSIL, and CC.
An asymptomatic 40-years old woman had Colonoscopy because of high serum level of CEA. Colonoscopy revealed rectal polypoid lesion 10 mm in size, which endoscopic diagnosis was high grade adenoma or ...intramucosal carcinoma. The lesion was located lower rectum to anal canal, ESD was performed. Resected specimen showed Tubular adenoma with severe atypia in elevated lesion, and anal intraepitherial neoplasia was adjacent to adenoma. She had a history of HPV infection. We should take care AIN during examining anal canal endoscopically, especially a patient have a history of HPV infection.
Gamma‐papillomaviruses, though traditionally classified as cutaneotropic, actual tissue tropism is largely unexplored. This study aimed to evaluate the tissue‐specific prevalence of two novel‐HPV 223 ...and 225 in samples of oral mucosa and keratinized epithelium of varied skin parts from 226 female and male subjects, with or without neoplastic/dysplastic lesions in oral cavity or cervix. The gamma‐human papillomavirus (gamma‐HPV) 223 and 225 DNA presences were determined by polymerase chain reaction (PCR) ursing the HPV type‐specific primers and confirmed by Sanger sequencing. Viral load in the HPV 223 and HPV 225 positive samples were determined by absolute real‐time quantification method. Alpha‐HPV DNA prevalence was also checked in oral mucosa to ascertain coinfection status. Novel HPV 223 was present in 4.4% (10/226) oral mucosal samples of the study population; interestingly all were females with no prevalence in their corresponding skin swab samples. Whereas, the prevalence of HPV 225 was found both in the skin and oral mucosa of 28.2% (N = 37/131) female and 17.9% (N = 17/95) male participants. Alongside, HPV 223 viral load was found to be significantly higher (p = 0.02 < 0.05) in the oral mucosa of diseased participants, whereas, HPV 225 viral load was higher in the oral mucosa of normal participants. Our results suggest that gamma‐HPV 223 has its prevalence only in the oral mucosal epithelium, whereas, HPV 225 has its prevalence on both mucosal and keratinized skin epithelium, indicating its dual tropism nature.
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