The Human papillomavirus /HPV is a virus that can infect the skin or mucous membranes (like the genitals, or inside the mouth) of humans. They cause warts. Some of them may cause cancer. There are over 100 different virus types in this group. About 40 virus types can be transmitted sexually. About 12-15 can cause cancer.
- Cervical cancer
- Factor in other cancers (Anal, Vaginal, Vulvar, Penile, Head and neck cancer (HPV-positive oropharyngeal cancer))
- Warts (genital, plantar, flat, Laryngeal papillomatosis), Epidermodysplasia verruciformis, Focal epithelial hyperplasia, Papilloma
age, sex, seasonality, etc
HPV Invasion + caption
Human papillomaviruses (HPVs) are ubiquitous DNA viruses that infect cutaneous and mucosal epithelia. A subset of HPVs infects the female genital tract, to induce cervical lesions that can progress to malignancy in some women. DNA from HPVs can be found in >94% of cervical carcinomas (CaCx) worldwide; this strong association suggests that it might be possible to develop either prophylaxis or therapies for cervical neoplasia, based on the manipulation of human immune responses against HPVs. This review examines the current research into human immune responses against HPVs in CaCx and the potential impact of this research on human health.
Human cellular immune responses against human papillomaviruses in cervical neoplasia, 1998
Unique Strains of SV40 in Commercial Poliovaccines from 1955 Not Readily Identifiable with Current Testing for SV40 Infection
PATIENT RISK FACTORS
TISSUE SPECIFIC RISK FACTORS
anatomical (due its structure)
vascular (due to the local circulation)
physiopathological (due to tissue function and activity)
Treatment of recalcitrant periungual warts with cimetidine in pediatrics.2010 Chern E, Cheng YW.J Dermatolog Treat. 2010 Sep;21(5):314-6.
- Viral warts, caused by human papilloma virus (HPV), are commonly seen in dermatology clinics. However, treatment for warts can be challenging, and there is no single method of treatment that is universally effective. Conventional therapies involve the physical destruction of lesions, including cryotherapy, electrodesiccation, CO2 laser, and topical keratolytic agents. Successful treatment of recalcitrant warts, especially periungual lesions and verruca plana of the face, had been limited with the conventional modalities. These painful procedures resulting in poor compliance, cosmetic disfiguration, and residual indolent lesions usually led to incomplete treatment. Use of high-dose cimetidine in the treatment of viral warts has been reported in the literature in recent years; however, with conflicting results. Herein, we present a 12-year-old girl with recalcitrant periungual warts, successfully treated with cimetidine for 4 months without subsequent recurrence and side effects.
Infection With Human Papillomavirus Alters Expression of the Small Proline Rich Proteins 2 and 3, 2004
- Human papillomavirus (HPV) does not induce lysis of infected keratinocytes, and the exact
mechanisms of viral escape are not known. As keratinocytes differentiate, the corniﬁed cell
envelope (CCE) develops, providing a protective barrier to the host. Our prior studies have
identiﬁed abnormalities in CCEs isolated from genital epithelium infected with HPV 11 (a lowrisk HPV type) and HPV 59 (a high-risk HPV type).
These abnormalities included reduced thickness and increased fragility compared to CCEs
in healthy epithelium. Transcription of loricrin is also reduced in HPV 11- and 59-infected epithelium. In this study, uninfected and HPV 11- or 59-infected human genital epithelium were examined for expression of the small proline rich proteins (SPRs), which serve as cross-linking proteins within the CCE. Limiting cycle RT-PCR was performed to detect the various SPR transcripts in HPV 11- and 59-infected, or uninfected epithelium. Immunohistochemical analysis and immunoblot assays were performed to analyze the distribution and quantity of SPR2A, SPR2B, and SPR3. SPR2B transcripts were moderately increased in the HPV 11- and 59-infected tissues and SPR3 transcripts were signiﬁcantly increased in HPV 11-infected tissues and minimally increased in HPV 59-infected tissues. SPR2B protein quantities were moderately increased while SPR2A was not signiﬁcantly changed.
SPR3 protein, while not present in uninfected epithelium, was detected in abundance in HPV
11-infected tissue. We conclude that low-risk and high-risk HPVs share the ability to alter expression of CCE proteins, although the exact mechanisms may differ. Expression of individual SPRs differed between these types and these alterations may play a role in fragility of CCEs in HPV infection
Human papillomavirus persistence and nutrients involved in the methylation pathway among a cohort of young women. 2002
Persistent oncogenic human papillomavirus (HPV) infection is associated with cervical dysplasia. Cofactors, such as nutrient status, may be required for the progression of HPV infection to neoplasia. HPV DNA methylation patterns in vitro have been shown to be associated with viral transcriptional activity. Folate, vitamin B12, vitamin B6, and methionine may function to prevent cervical cancer through their role in DNA methylation. This study was conducted to examine the relationship of dietary intake of folate, vitamin B12, vitamin B6, and methionine, as well as circulating levels of folate and vitamin B12 to HPV persistence. Oncogenic HPV status was determined at baseline and at approximately 3 and 9 months postbaseline. Multivariate logistic regression analysis was used to determine the adjusted odds ratios for persistent HPV infection associated with each tertile of individual nutrient among 201 women with a persistent or intermittent HPV infection. Circulating vitamin B12 levels were inversely associated with HPV persistence (P for trend, 0.037) after adjusting for age, age at first intercourse, marital status, cigarette smoking status, race, and body mass index. In addition, women with circulating levels in the highest tertile (>493.2 pg/ml) of vitamin B12 were less likely to have a persistent infection (adjusted odds ratio = 0.4; 95% confidence interval = 0.17-0.96). No significant associations were observed between HPV persistence and dietary intake of folate, vitamin B12, vitamin B6, or methionine from food alone or from food and supplements combined or from circulating folate. These data suggest a role for circulating vitamin B12 in early cervical carcinogenesis.
The role of diet and nutrition in cervical carcinogenesis: a review of recent evidence. 2005
- Our objective was to provide an update on recent epidemiologic evidence about the role of diet and nutrition on the risk of human papillomavirus (HPV) persistence and cervical neoplasia, taking HPV into account.
Association of methylenetetrahydrofolate reductase polymorphism C677T and dietary folate with the risk of cervical dysplasia. 2001
- Methylenetetrahydrofolate reductase (MTHFR) catalyzes the synthesis of 5-methyltetrahydrofolate, which is involved in the methylation of homocysteine to methionine.
Infezioni virali in ginecologia: un problema risolto? 2016
- The aim of this observational study was to evaluate the effectiveness of a dietary integrator containing methionine, zinc, Echinacea angustifolia and E.
A relationship between methylenetetrahydrofolate reductase variants and the development of invasive cervical cancer. 2003
- Methylenetetrahydrofolate reductase (MTHFR) is a critical enzyme regulating the metabolism of folate and methionine, the important components of DNA synthesis and methylation.
Human cellular immune responses against human papillomaviruses in cervical neoplasia, 1998
Human papillomavirus (HPV) infection and replication in cervical epithelial cells. (a) The normal cervix has a (narrow) transformation zone in which there is an abrupt transition from a columnar epithelium (sometimes via a metaplastic epithelium) to a squamous epithelium; HPVs are probably most infectious to cells that are close to this junction. (b) HPV viruses gain access to the basal epithelial cells of the cervix via the vagina (for example, during sexual intercourse), where they replicate episomally (outside the host chromosome in the cytoplasm) and express the (early) viral genes E1, E2, E4, E5, E6 and E7. © The infected basal cells, which show signs of cell disruption as a result of the viral infection, continue their differentiation and migration to the epithelial surface, where (d) the (now) squamous cells start to express the late HPV genes LI and L2. Infectious virus particles are formed and shed into the lumen of the vagina. (e) HPV infection (particularly with the high-risk types) can progress to: (1) HPV-induced mild dysplasia, (2) the final stages of cervical intraepithelial neoplasia (CIN3) and, eventually, (3) invasive cervical cancer (CaCx), when the basement membrane is breached by the cells, allowing local spread and also distant metastasis. (f) In transformed epithelial cells, HPV genes are integrated into the host chromosomes, with expression of (the oncogenic) E6 and E7 proteins, which bind to the tumour-suppressor proteins p53 and Rb (fig001smc).