Papilloma vírus in vitro, Az emberi 6-os herpeszvírus = Human herpesvirus 6 - Repository of the Academy's Library

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Discovery InLudwik Gross reported that a filterable infectious agent could cause salivary cancer in laboratory mice Gross, ; Stewart et al. The discovery spurred renewed interest in the idea that viral infections might be a major cause of cancer in humans.

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By the late s, various investigators had succeeded in developing cell culture systems for analysing the transforming activities of murine polyomavirus in vitro. Inthe first two naturally human-tropic polyomaviruses were discovered in specimens from immunocompromised patients Gardner et al.

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Reports in the past four years have revealed the existence of seven more human polyomaviruses. Perhaps the most intriguing of the new species, named Merkel cell polyomavirus MCVwas discovered through a directed genomic search of an unusual form of skin cancer, Merkel cell carcinoma MCC Feng et al.

Az emberi 6-os herpeszvírus = Human herpesvirus 6 - Repository of the Academy's Library

Another new polyomavirus, trichodysplasia spinulosa-associated polyomavirus TSVwas isolated from a rare hyperplastic but non-neoplastic trichodysplasia spinulosa skin tumour that can occur in transplant patients van der Meijden et al. Little is currently known about the cancer-causing potential of TSV. Taxonomy and phylogeny The exterior structure of the non-enveloped capsids of members of the viral family Polyomaviridae papilloma vírus in vitro strikingly similar to the capsids of a different family of non-enveloped viruses called the Papillomaviridae.

Based on these considerations, the two virus groups were originally classified within a single papilloma vírus in vitro, hiv és májrák Papovaviridae a sigla condensation of PApillomavirus POlyomavirus simian VAcuolating. However, sequencing of the genomes of various polyomaviruses and papillomaviruses revealed essentially no detectable sequence homology between the two virus groups and furthermore showed that the two groups had dramatically different genetic organization.

Since the sequencing results indicate that polyomaviruses and papillomaviruses probably never shared a common viral ancestor, they were officially split into separate viral families. Interestingly, several recent reports suggest that polyomaviruses and papillomaviruses may occasionally recombine with one another to produce viable chimeric viruses with mixed genetic characteristics of both families Woolford et al.

Another recent report documenting a novel viral species that infects eels suggests that polyomaviruses might also recombine with members of other families of DNA viruses to produce viable chimeric progeny Mizutani et al. The taxonomy of these apparently chimeric viral species is currently undefined.

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A recent proposal that is currently being reviewed by the International Committee on Taxonomy of Viruses suggests that the various members of the family Polyomaviridae be grouped into separate genera Johne et al.

If approved, this would result in the division of the current sole genus Polyomavirus into three genera: Papilloma vírus in vitro, Wukipolyomavirus, and Avipolyomavirus.

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The first two genera encompass all the currently known human- and primate-tropic species, while the third genus includes species thought to be tropic only for birds.

Phylogenetic analyses of BKV and JCV isolates from different populations worldwide have shown that the two virus species exhibit a geographical pattern of genetic drift that closely resembles proposed patterns of prehistoric human migration reviewed in Yogo et al.

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Phylogenetic trees based on the nucleotide or amino papilloma vírus in vitro sequences of individual viral gene products give similar results, suggesting that the members of the SV40 cluster diverged from one another relatively recently, while the split between MCV and members of the SV40 cluster occurred papilloma vírus in vitro the much more distant past. Phylogenetic tree of known polyomavirus species 3.

Structure of the virion The exterior surface of the polyomavirus virion is a naked protein capsid composed entirely of a single virally encoded protein called capsid viral protein 1 VP1 Stehle et al.

VP1 subunits are folded into a classic eight-stranded β jellyroll fold that is shared among a wide variety of viral capsid proteins and the cellular protein nucleoplasmin Stehle et al.

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The jellyroll, which forms the core of the pentameric VP1 interface, is arranged perpendicular to the spherical virion, such that the assembled virion has a distinctive knobby appearance. In all extensively studied examples, it appears that polyomavirus infectious entry requires interactions between VP1 and one or more cellular glycans that carry at least one sialic acid residue.

The loops that form the receptor binding pocket vary extensively between polyomavirus species, and even papilloma vírus in vitro closely related polyomavirus hasi rák cie 10 Luo et al.

This variation may reflect selective pressure to evade recognition by antibodies that occlude the receptor binding site.

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The floor of the canyons between the capsomer knobs is formed primarily by N- and C-terminal arms of VP1. The arms are stabilized by disulfide bonds between neighbouring VP1 molecules. The fully mature virion shows a remarkably high degree of stability and can remain fully infectious even after aggressive insults, such as heating at 75 °C for 1 hour Lelie et al.

This high degree of virion stability raises the possibility that polyomaviruses might be transmitted environmentally or via lightly cooked meat products reviewed in zur Hausen, Purified VP1 can spontaneously self-assemble into virus-like particles VLPs that closely resemble the native virion Salunke et al.

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Such VLPs have been widely used for serological analyses of polyomavirus epidemiology Hamilton et al. Purified polyomavirus VLPs can be immunogenic when administered to laboratory animals, raising serum antibody responses capable of neutralizing native virions in vitro Goldmann et al. VLPs can even be humorally immunogenic in mice in the absence of functional T-cell immunity Vlastos et al.

This suggests that polyomaviruses might be a suitable target for the development of VLP-based preventive vaccines, similar to the highly successful VLP-based vaccines against hepatitis B virus and human papillomaviruses HPV. Genomic organization, gene products, and replication The circular ~5 kb dsDNA polyomavirus genome is roughly divided into two oppositely schistosomiasis zyklus transcriptional units separated by a non-coding control region NCCR reviewed in Gu et al.

The term T-antigen historically derives from their expression in SVinduced tumours Rapp et al. Although T-antigen sequences vary among the mammalian polyomavirus species, the overall arrangement of major functional domains of the singly spliced LT gene is broadly conserved and sT is expressed from an unspliced open reading frame encoding a protein of low relative molecular mass 18—20 kDa.


The splice donor used for mRNAs encoding LT is within the sT open reading frame, such that sT and all LT isoforms share a common leader peptide sequence, typically about 80 amino acids long.

In addition, many polyomavirus species express multiply spliced transcripts encoding various T-antigen isoforms. The NCCR is highly variable between, and even within, polyomavirus species. The expression of un-terminated late mRNAs with perfect complementarity to early T-antigen mRNAs is thought to play an important role in the regulation of the shift from expression of the T-antigens early after infection to the expression of capsid proteins during the productive late phase of infection reviewed in Gu et al.

The early-to-late shift may also be partially controlled by expression of microRNAs that appear to be encoded on late strand transcripts transiting the early region Sullivan et al. These microRNAs may be capable of antagonizing early gene expression and might also exert regulatory effects on the host cell Bauman et al. The structure of these conformational changes and DNA binding for LT double hexamers has been solved by crystallography Li et al. The species-specific ability of LT to recruit DNA polymerase α-primases of various hosts papilloma vírus in vitro to be a major determinant of polyomavirus host range see below.

Proposed roles for agnoproteins include regulation of viral gene expression, virion assembly, cell lysis, and dysregulation of a wide variety of cellular processes Suzuki et al.

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Viral life-cycle Like other non-enveloped virus families, polyomaviruses are believed to breach host-cell membranes papilloma vírus in vitro internalization via endocytic pathways. For polyomaviruses whose infectious entry pathways have been extensively studied, a common feature appears to be the engagement of cell-surface glycans that carry at least one sialic acid residue Tsai et al. In the cases of murine polyomavirus, SV40, and BKV, the entry receptor is one or more types of sialylated lipids called gangliosides.


The target gangliosides appear to be widely distributed on a variety of cell types since these viruses, or reporter vectors based on them, can infect or transduce a wide range of cell lines from various species Nakanishi et al. Thus, receptor binding and subsequent steps in the infectious entry process are unlikely to be major determinants of host or tissue tropism.

For MCV, there is controversy about whether the sialylated glycans required for infectious entry are displayed in the form of gangliosides or in association with protein Erickson et al.

In addition to the sialylated glycan co-receptor, MCV also appears to require interactions with a different highly widespread form of cellular glycan called heparan sulfate. The expression of the unique entry receptors of JCV may dictate its tropism for cells of the central nervous system in vivo see Section 1.

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After engagement of the cognate receptor, polyomaviruses are endocytosed and traffic through the endoplasmic reticulum, where cellular factors facilitate compromise of the cellular lipid bilayer, allowing escape of the viral genome into the cytoplasm. In permissive cells, papilloma vírus in vitro early genes target host-cell signalling to drive cell-cycle progression.

By promoting cellular expression of DNA replication factors, replication of the episomal viral DNA is facilitated, possibly through a rolling circle replication mechanism Bjursell, Expression of the LT antigen can concurrently lead to expression of late gene capsid proteins.

Assembly of high levels of encapsidated virus results in active lysis of the host cell.