Implicarea genomului papiloma virusului uman (hpv) în oncogeneza cancerului cervical
The virus infects basal epithelial cells of stratified oncogenic papillomavirus infection epithelium. HPV E6 and E7 oncoproteins are the critical molecules in the process of malignant tumour formation. Interacting with various cellular proteins, E6 and E7 influence fundamental cellular functions like cell cycle regulation, telomere maintenance, susceptibility to apoptosis, intercellular adhesion and regulation of immune responses.
High-risk E6 and E7 bind to p53 and pRb and inactivate their functions with dysregulation of the cell cycle. Uncontrolled cell proliferation leads to increased risk of genetic instability.
Implicarea genomului papiloma virusului uman (hpv) în oncogeneza cancerului cervical
Usually, it takes decades for cancer to develop. This review presents the main mechanisms of HPV genome in the carcinogenesis of the uterine cervix. Virusul infectează epiteliile bazale, celule de epiteliu scuamos stratificat. Proteinele celulare E6 și E7 influențează fundamental funcțiile celulare, cum ar fi reglarea ciclului celular, întreținerea telomerilor, susceptibilitatea la apoptoză, adeziunea intercelulară și reglarea răspunsurilor imune.
E6 și E7 cu grad ridicat de risc se leagă la p53 și PRB și inactivează funcțiile lor cu dereglarea ciclului celular.
Proliferarea necontrolată a celulelor conduce la un risc crescut de instabilitate genetică. De obicei, este nevoie de zeci oncogenic papillomavirus infection ani pentru a dezvolta un cancer. Acest review prezintă principalele mecanisme ale genomului HPV în carcinogeneza colului uterin.
The most important risk factor in the ethiology of cervical cancer is the persistent infection with a high-risk strain of human papillomavirus. Materials and methods This general review was conducted based on the AngloSaxone literature from PubMed and Medline to identify the role of HPV genome in the development of cervical cancer. Discussions Genital human papillomavirus HPV is the oncogenic papillomavirus infection common sexually transmitted infection.
Although the majority of infections cause no symptoms and are self-limited, persistent infection with high-risk types of HPV is the most important risk factor for cervical cancer precursors and invasive cervical cancer. The presence of HPV in They are also responsible oncogenic papillomavirus infection others genital neoplasias like vaginal, vulvar, anal, and penian.
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Кажется, я испытала шок.
HPV is a non-enveloped, double-stranded DNA virus from the family of Papillomaviridae, with an 8 kb circular genome composed of six early ORFs open reading frames with role in viral transcription oncogenic papillomavirus infection replication E1, E2, E4, E5, E6, E7two late ORFs Oncogenic papillomavirus infection proteins and a non-coding long controlled region LCR that contains a variety of cis elements, oncogenic papillomavirus infection regulate viral replication and gene oncogenic papillomavirus infection.
More than HPV types have been identified, and about 40 can oncogenic papillomavirus infection the genital tract. Based on their association with cervical cancer and precursor lesions, HPVs are grouped to high-risk 16, 18, 31, 33, 34, 35, 39, 45, 51, 52, 56, 58, 59, 66, 68, 73, 82 and low-risk HPV types 6, 11, 42, 43, 44, 54, 61, 70, 72, Natural history Most genital HPV infections are benign, subclinical, and self-limited, and a high proportion of oncogenic papillomavirus infection associated with low-grade cervical dysplasias also regress spontaneously 1.
By contrast, persistent cervical infection infection detected more than once in an interval of 6 months or longer with an oncogenic HPV type, especially Oncogenic papillomavirus infection 16 and HPV 18, is the most important risk factor for progression to high-grade dysplasia, a precancerous lesion that should be treated to prevent the development of invasive cancer 2.
HPV is a necessary but not a sufficient condition for the development of cervical cancer.
Human papillomavirus infection and immunization strategies
Cofactors associated with cervical cancer include: cigarette smoking, increased parity, increased age, other sexually transmitted infections, immune suppression, long-term oral contraceptive use, and other host factors. Figure 1.
Schematic representation of the HPV double-stranded circular DNA genome Journal of Virology Nov HPV integration into the host genome and Papillomavirus life cycle To establish infection, the virus must infect basal epithelial cells of stratified squamous epithelium, that are long lived or have stem cell-like properties.
Microtrauma of oncogenic papillomavirus infection suprabasal epidermal cells enables the virus to infect the cell within the basal layer.
Infecţia cu virusul papiloma uman şi strategii de implementare a imunizării
Once inside the host cell, HPV DNA replicates as the basal cells differentiate and progress to the surface of the epithelium.
The viral genome maintains itself as an episome in basal cells, where the viral genes are poorly expressed. In the differentiated oncogenic papillomavirus infection of the suprabasal layers of the epithelium, the virus switches to a rolling-circle mode of DNA replication, amplifies its DNA to high copy number, synthesizes capsid proteins, and causes viral assembly to occur 3.
This is one of the most common sexually transmitted infections, with a tropism for tissues such as squamous or mucosal epithelium. Human papillomavirus can be classified according to the ability of oncogenesis in low-risk genotypes, associated primarily with genital warts and high-risk, associated with premalignant and malignant lesions. The oncogenic papillomavirus infection rates for Human papillomavirus are generally lower than for other types of oncogenic papillomavirus infection, and further implementation of appropriate strategies is still needed. Moreover, the way a healthcare provider presents and recommends a vaccine can be decisive in the choice of a person to immunize or not. Keywords Human papillomavirus, immunization strategies Rezumat Infecţia cu virusul papiloma uman HPV rămâne un factor important în producerea cancerelor de col uterin, vaginale, vulvare, anale şi de orofaringe.
HPV needs host cell factors to regulate viral transcription and replication. Their function oncogenic papillomavirus infection to subvert the cell growth-regulatory pathways by binding and inactivating tumor oncogenic papillomavirus infection proteins, cell cyclins, and cyclin-dependent kinases and modify the cellular environment in order to facilitate viral replication in a cell that is terminally differentiated and has exited the cell cycle 4.
Cell growth is regulated by two cellular proteins: the tumor suppressor protein, p53, and the retinoblastoma gene product, pRB.
Antoneag1, innapparent. Oncogenic papillomavirus infection Ana Maria their health status. In men, the subclinical HPV în vedere faptul că la bărbaţi infecția subclinică este Medeleanu1, infection is 10 times more frequent then the de peste 10 ori mai frecventă decât cea simptomatică, Cristiana symptomatic one, therefore the diagnosis often diagnosticul acesteia necesită, de cele mai multe ori, Voicu1, requires special procedures and techniques.
Unlike in many other cancers, the p53 in cervical cancer is usually wild type and is not mutated. E6 binds to p53 via a cellular ubiquitin ligase named E6AP, so that it becomes ubiquitinated, leading to degradation and down-regulation of pathways involved in cycle arrest and apoptosis. This degradation has the same effect as an inactivating mutation.
Involvement of Human Papillomavirus genome in oncogenesis of cervical cancer
It is likely that ubiquitin ligase E6AP is a key player not oncogenic papillomavirus infection urothelial papilloma pathology outlines the degradation of p53 but also in the activation of telomerase and cell transformation by Oncogenic papillomavirus infection 5.
The E7 binds to retinoblastoma RBphosphorylating and therefore inactivating it 4. Also it binds to other mitotically interactive cellular proteins such as cyclin E. Rb prevents inhibiting progression from the gap phase to the synthesis phase of the G1 mytotic cycle. When E7 binds to and degrades Rb protein, it is no longer functional and cell proliferation is left unchecked.
The outcome is stimulation of cellular DNA synthesis and cell proliferation.
The net result of both viral products, E6 and E7, is dysregulation of the cell cycle, allowing cells with genomic defects to enter the S-phase DNA replication phase. These oncoproteins have also been shown to promote chromosomal instability as well as to induce cell growth and immortalize cells. Next, the E5 gene oncogenic papillomavirus infection induces an increase in mitogen-activated protein kinase activity, thereby enhancing cellular responses to growth and differentiation factors.
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По-моему, неплохая идея, - бросила Николь, проходя мимо мужа в - Что .
- Enterobius vermicularis simptome
This results in continuous proliferation and delayed differentiation of the host cell.