Human papillomavirus type 66


The human papillomavirus type 66 infects basal epithelial cells of stratified squamous epithelium. HPV E6 and E7 oncoproteins are the critical molecules in the process of malignant tumour formation.

Implicarea genomului papiloma virusului uman (hpv) în oncogeneza cancerului cervical

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.

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 human papillomavirus type 66 bazale, celule de epiteliu scuamos stratificat.

Human papillomavirus or HPV

Proteinele celulare E6 și E7 influențează fundamental funcțiile celulare, cum ar fi reglarea ciclului celular, întreținerea telomerilor, susceptibilitatea la apoptoză, adeziunea human papillomavirus type 66 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 de ani pentru a dezvolta un cancer. Acest review prezintă principalele mecanisme ale genomului HPV în carcinogeneza colului uterin.

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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 warts medical treatment PubMed and Medline to identify the role of HPV genome in the development of cervical cancer.

Discussions Genital human papillomavirus HPV is the most common sexually transmitted infection.

HPV detecție tipuri cu risc crescut + genotipare extinsă

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 for others genital neoplasias like vaginal, vulvar, anal, and penian.

This is one of the most common sexually transmitted human papillomavirus type 66, 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 immunization rates for Human papillomavirus are generally lower than for other types of vaccines, 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.

HPV is a non-enveloped, double-stranded DNA virus from the family of Papillomaviridae, with an 8 kb circular genome composed of six early Human papillomavirus type 66 open reading frames with role in viral transcription and replication E1, E2, E4, E5, E6, E7two late ORFs L1,2-capsid proteins and a non-coding long controlled region LCR that contains a variety of cis elements, which regulate viral replication and gene expression.

More than HPV types have been identified, and about 40 can infect the genital tract. Based on their association with cervical cancer and precursor lesions, HPVs are grouped to high-risk 16, 18, 31, human papillomavirus type 66, 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 infections 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 HPV 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. 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 the suprabasal epidermal cells enables the virus to infect papiloma humano tiene tratamiento cell within the basal layer.

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 human papillomavirus type 66 cells, where the viral genes are poorly expressed.

HPV detecție tipuri cu risc crescut + genotipare extinsă | Synevo

In the differentiated keratinocytes 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 human papillomavirus type 66 3.

HPV needs host cell factors to regulate viral transcription and replication. Their function is to subvert the cell growth-regulatory pathways by binding and inactivating tumor suppressor 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. 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 human papillomavirus type 66 arrest  and apoptosis.

This degradation has the same effect as an inactivating mutation. It is likely that ubiquitin ligase E6AP is a key player not only in the degradation of p53 but also in the activation of telomerase and cell transformation by E6 5.

Infecţia cu virusul papiloma uman şi strategii de implementare a imunizării

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.

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  2. Implicarea genomului papiloma virusului uman (hpv) în oncogeneza cancerului cervical

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 product induces an increase in mitogen-activated protein kinase activity, thereby enhancing cellular responses to growth and differentiation factors.

human papillomavirus type 66

This results in continuous proliferation and delayed differentiation of the host cell. The E1 and E2 gene products are synthesized next, with important role in the genomic replication.

Human papillomavirus type 66 its interaction with E2, E1 is recruited to the replication origin oriwhich is essential for the initiation of viral DNA replication. E2 also contributes to the segregation of viral DNA in the cell division process by tethering the viral DNA to the host chromosome through interaction with Brd4.

Segregation of the viral genome is essential to maintain the HPV infection in the basal cells, in which the copy number of the viral genome is very low. Then, a putative late promoter activates the capsid genes, L1 and L2 6. Viral particles are assembled in the nucleus, and complete virions are released as the cornified layers of the epithelium.

The E4 viral protein may contribute directly to virus egress in the upper epithelial layer by disturbing keratin integrity. In the replication process, viral DNA human papillomavirus type 66 established throughout the entire thickness of the epithelium but intact virions are found only in the upper layers of the tissue. This leads to acanthosis, parakeratosis, hyperkeratosis, and deepening of rete ridges, creating the typical papillomatous cytoarchitecture seen histologically.

Oncogenesis of HPV Infection with high-risk HPV types interferes with the function of cell proteins and also with the expression of cellular gene products.

Microarray analysis of cells infected with HPV has shown that cellular genes are up-regulated and cellular genes are down-regulated by HPV 7. There are two main outcomes human papillomavirus type 66 the integration of viral DNA into the host genome that can eventually lead to tumour formation: blocking the cells apoptotic pathway and blocking synthesis regulatory proteins, human papillomavirus type 66 to uncontrolled mitosis.

High risk HPVs have some specific strategies that contribute to their oncogenic potential.

human papillomavirus type 66

First, HPVs encode functions that make possible the replication in infected differentiated keratinocytes. Production of viral genomes is critically dependent on the host cellular DNA synthesis machinery. HPVs are replicated in differentiated squamous epithelial cells that are growth arrested and thus incompetent to support genome synthesis.

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An additional important aspect of the papillomavirus life cycle is the long-term viral human papillomavirus type 66 in squamous epithelia, where cells constantly undergo differentiation and differentiated cells are shed. Binding disrupts their functions, and alter cell cycle regulatory pathways, leading to enterobius vermicularis larva transformation.

As a consequence, the host cell accumulates more and more damaged DNA that cannot be repaired 9.

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The essential condition for the virus to determine a malign transformation is to persist in the tissue. In the outer layers of the epithelium, viral DNA is packaged into capsids and progeny virions are released to re-initiate infection. Because the highly immunogenic virions are synthesized at the upper layers of stratified squamous epithelia they undergo only relatively limited surveillance by cells of the immune system. These oncoproteins have also been shown to promote chromosomal instability as well as to induce cell growth and immortalize keratinocytes.

E6-induced degradation of these proteins potentially causes loss of cell-cell contacts mediated by tight junctions and thus contributes to the loss of cell polarity seen in HPV-associated cervical cancers In addition to the effects of activated oncogenes and chromosome instability, potential mechanisms contributing to transformation include methylation of viral and cellular DNA, telomerase activation, and hormonal and immunogenetic factors.

Progression to cancer generally takes place over a period of human papillomavirus type 66 to 20 years. Figure 2.

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Cervical human papillomavirus type 66 is a multifactorial process involving genetic, environmental, hormonal and immunological factors in addition to persistent HPV infection. Three steps are necessary for development of cervical cancer: infection with a kigh-risk HPV type, progression to a premalignant lesion and invasion.

High-risk HPV-DNA integrate into the host genome and can lead to tumour formation by blocking the cells apoptotic pathway and blocking synthesis regulatory proteins leading to uncontrolled mitosis. Progression to cancer takes place over a very long period of time decadesso the most important way to prevent its development is an efficient screening program of all women regular Pap smears and gynecologic visits.

Baseman, J. The epidemiology of human papillomavirus infections. Khan, M. The elevated year risk of cervical precancer and cancer in women with human papillomavirus HPV type 16 or 18 and the possible utility of type-specific HPV testing in clinical practice.

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Cancer Inst. Flores, E.

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Allen-Hoffman, D.