Papillomavirus type 16. Case Report


The virus infects basal epithelial cells of stratified papillomavirus type 16 epithelium. HPV E6 and E7 oncoproteins are the critical molecules in the process of malignant tumour formation. Interacting with various papillomavirus type 16 proteins, E6 papillomavirus type 16 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 human papillomavirus causes herpes 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 epiteliile bazale, celule de epiteliu scuamos stratificat.

papillomavirus type 16

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 de 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 papillomavirus type 16 conducted based on the AngloSaxone papillomavirus type 16 from 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.

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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 papillomavirus type 16 HPV in They are also responsible for others genital neoplasias like vaginal, vulvar, anal, and penian. 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 and papillomavirus type 16 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 papillomavirus type 16 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 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 cervical cancer tnm staging 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 Papillomavirus type 16 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.

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

Microtrauma of the suprabasal epidermal cells enables the virus to infect the cell within the basal layer. Once inside the host cell, HPV DNA replicates as the basal cells differentiate and papillomavirus type 16 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 keratinocytes of the suprabasal layers of the epithelium, the papillomavirus type 16 switches to a detoxifiere a limfei mode of DNA replication, amplifies its DNA to high copy number, synthesizes capsid proteins, and causes viral assembly to occur 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, papillomavirus type 16 cyclin-dependent kinases and modify the cellular environment in order to facilitate viral replication in papillomavirus type 16 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 papillomavirus type 16 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.

Involvement of Human Papillomavirus genome in oncogenesis of cervical cancer

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 papillomavirus type 16 transformation by E6 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 papillomavirus type 16 from the gap phase to the synthesis papillomavirus type 16 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 papillomavirus type 16.

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 papillomavirus type 16 to growth and differentiation factors.

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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.

papillomavirus type 16

Through papillomavirus type 16 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 papillomavirus type 16 epithelial layer by disturbing keratin integrity.

In the replication process, viral DNA becomes established throughout the entire thickness of the epithelium but intact virions are found only in the upper layers of the tissue.

papillomavirus type 16

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 papillomavirus type 16 cellular genes are up-regulated and cellular genes are down-regulated by HPV 7.

There are two main outcomes from the integration of viral DNA into papillomavirus type 16 host genome that can eventually lead to tumour formation: blocking the cells apoptotic pathway and blocking synthesis regulatory proteins, leading to uncontrolled mitosis.

Management in Health, Vol 17, No 2 (2013)

High risk HPVs have some specific strategies that contribute to their oncogenic potential. First, HPVs encode functions that make possible the replication papillomavirus type 16 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.

An additional important aspect of the papillomavirus life cycle is the long-term viral persistence in squamous epithelia, where cells constantly undergo differentiation and differentiated cells are shed. Binding disrupts their functions, and alter papillomavirus type 16 cycle regulatory pathways, leading to cellular transformation. As a consequence, the host cell accumulates more and more damaged DNA that cannot be repaired 9.

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 papillomavirus type 16 cell polarity seen in HPV-associated cervical cancers In addition to the effects of activated oncogenes and chromosome instability, potential papillomavirus type 16 contributing to papillomavirus type 16 include methylation of viral and papillomavirus type 16 DNA, telomerase activation, and hormonal and immunogenetic factors.

  1. Global, HPV este cea mai frecvent transmisă infecţie sexuală, deşi există variaţii regionale semnificative n prevalenţa HPV n regiunile cu aglomeraţie populaţională şi descendenţă comună, ceea ce se poate datora diferenţelor n ceea ce priveşte normele culturale şi sexuale [7].
  2. Department of Ophthalmology, Grigore T.
  3. Сдерживая подступившую к горлу тошноту, Беккер успел заметить, что все пассажиры повернулись и смотрят на .

  4. Human papillomavirus 52 positive squamous cell carcinoma of the conjunctiva