Basal cells comprise the proliferating cellular component of stratified epithelia, in which the viral genome is established when a low copy number, nuclear plasmid and early genes are expressed preferentially although at low levels ( Stoler & Broker, 1986 Schneider et al., 1987 Frattini et al., 1996 Oguchi et al., 2000). Although several potential receptors have been reported, it is unclear which of them is of physiological importance (see Section 1.1.5( g)). The life cycle is thought to be initiated by the infection of basal epithelial cells, presumably at sites of injury. The viral life cycle is linked to the differentiation of the infected epithelial cell (see Figures 2 and 3). Papillomaviruses are highly epitheliotropic specifically, they establish productive infections only within stratified epithelia of the skin, the anogenital tract and the oral cavity. The L1 and L2 proteins assemble in capsomers, which form icosahedral capsids around the viral genome during the generation of progeny virions ( Fehrmann & Laimins, 2003). During the viral life cycle, E6 and E7 facilitate stable maintenance of viral episomes and stimulate differentiating cells to re-enter the S phase. ![]() The E6 and E7 proteins target a number of negative regulators of the cell cycle, primarily p105Rb and p53, respectively. E4, despite its name, is believed to be involved in the late stages of the life cycle of the virus and E5 may function during both early and late phases. The E1 and E2 proteins of HPV act as factors that recognize the origin of replication E2 protein is also the main regulator of viral gene transcription. The genome of the high-risk HPV 31 Modified. The ability to target the retinoblastoma (Rb) family of proteins and p53 and to induce telomerase are some of the critical events that contribute to the development of malignancy. Striking progress has been made in defining the activities of viral oncoproteins from high-risk genital HPVs, in particular HPVs 16 and 18, that promote the disruption of normal cell-cycle control. Molecular studies now provide a coherent picture of the mechanisms that regulate viral gene expression and replication nevertheless, gaps in the understanding of HPV biology remain. Early evidence suggests that HPV types, as defined by DNA sequencing, also remain serologically distinct. The availability of complete and partial genomic sequences from a wide variety of HPV types has enabled the establishment of a new taxonomic structure and has provided a window to study the co-evolution of papillomaviruses with their primate hosts. However, only in the late 1990s did propagation of viruses in organotypic cultures make the first attempts at viral genetics possible. The advent of molecular cloning of HPV genomes in the early 1980s provided the first opportunity to study individual viral genes. Understanding of the biology of papillomavirus infection was hindered by the lack of tissue culture systems to propagate the viruses, the lack of animal models for HPVs and difficulties in finding animal models of natural infection. Similarly, all papillomaviruses have a non-enveloped icosahedral capsid. A double-stranded circular DNA genome encodes approximately eight open-reading frames (ORFs). The potential associations of HPVs with these and other cancers are discussed in other sections.Īll papillomaviruses share a common genetic structure that is distinct from that of polyomaviruses. ![]() A number of HPVs have been found to be present in skin cancers in patients who have epidermodysplasia verruciformis (EV) these types are also found in both non-melanoma skin cancers and normal skin. These other types are associated with other anogenital and oropharyngeal cancers. Many types of HPV have been found in cervical cancers, while others are found rarely or not at all in large series of cancers, which gives rise to the nomenclature of ‘high-’ and ‘low-risk’ HPVs. ![]() More than 100 types of human papillomaviruses (HPVs) have been identified and approximately half of them infect the genital tract. Only bovine papillomaviruses (BPVs) 1 and 2 are known to infect mesenchymal tissues and to show cross-species transmission. Papillomaviruses are small, non-enveloped, epitheliotropic, double-stranded DNA viruses that infect mucosal and cutaneous epithelia in a wide variety of higher vertebrates in a species-specific manner and induce cellular proliferation.
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