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Microbiology Spectrum Aug 2016Individuals with inherited immunodeficiencies, autoimmune disorders, organ or bone marrow transplantation, or infection with human immunodeficiency virus (HIV) are at... (Review)
Review
Individuals with inherited immunodeficiencies, autoimmune disorders, organ or bone marrow transplantation, or infection with human immunodeficiency virus (HIV) are at increased risk of infection with both low-risk and high-risk human papillomavirus (HPV) types. Chronic immunosuppression provides an environment for persistent HPV infection which carries a higher risk of malignant transformation. Screening guidelines have been developed or advocated for processes that have detectable premalignant lesions, such as anal cancer or cervical cancer. For other anatomic locations, such as cutaneous, penile, and oropharyngeal, a biopsy of suspicious lesions is necessary for diagnosis. HPV cannot be cultured from clinical specimens in the laboratory, and diagnosis relies on cytologic, histologic, or molecular methods.
Topics: Clinical Laboratory Techniques; Diagnostic Tests, Routine; Disease Susceptibility; Humans; Immunocompromised Host; Papillomaviridae; Papillomavirus Infections
PubMed: 27726787
DOI: 10.1128/microbiolspec.DMIH2-0001-2015 -
Clinical Science (London, England :... May 2006HPVs (human papillomaviruses) infect epithelial cells and cause a variety of lesions ranging from common warts/verrucas to cervical neoplasia and cancer. Over 100... (Review)
Review
HPVs (human papillomaviruses) infect epithelial cells and cause a variety of lesions ranging from common warts/verrucas to cervical neoplasia and cancer. Over 100 different HPV types have been identified so far, with a subset of these being classified as high risk. High-risk HPV DNA is found in almost all cervical cancers (>99.7%), with HPV16 being the most prevalent type in both low-grade disease and cervical neoplasia. Productive infection by high-risk HPV types is manifest as cervical flat warts or condyloma that shed infectious virions from their surface. Viral genomes are maintained as episomes in the basal layer, with viral gene expression being tightly controlled as the infected cells move towards the epithelial surface. The pattern of viral gene expression in low-grade cervical lesions resembles that seen in productive warts caused by other HPV types. High-grade neoplasia represents an abortive infection in which viral gene expression becomes deregulated, and the normal life cycle of the virus cannot be completed. Most cervical cancers arise within the cervical transformation zone at the squamous/columnar junction, and it has been suggested that this is a site where productive infection may be inefficiently supported. The high-risk E6 and E7 proteins drive cell proliferation through their association with PDZ domain proteins and Rb (retinoblastoma), and contribute to neoplastic progression, whereas E6-mediated p53 degradation prevents the normal repair of chance mutations in the cellular genome. Cancers usually arise in individuals who fail to resolve their infection and who retain oncogene expression for years or decades. In most individuals, immune regression eventually leads to clearance of the virus, or to its maintenance in a latent or asymptomatic state in the basal cells.
Topics: Disease Progression; Female; Humans; Papillomaviridae; Papillomavirus Infections; Precancerous Conditions; Uterine Cervical Neoplasms; Virus Latency
PubMed: 16597322
DOI: 10.1042/CS20050369 -
Acta Cytologica 2019The cutaneous human papillomavirus (HPV), mostly from β- and γ-HPV genus, is ubiquitously distributed throughout the human body and may be part of the commensal flora.... (Review)
Review
The cutaneous human papillomavirus (HPV), mostly from β- and γ-HPV genus, is ubiquitously distributed throughout the human body and may be part of the commensal flora. The association of β-HPVs and cutaneous squamous cell carcinoma (cSCC) development was initially reported in patients with the rare genetic disorder Epidermodysplasia verruciformis. Likewise, immunosuppressed organ transplant recipients have an increased susceptibility to β-HPV infections in the skin as well as to cSCC development. Although ultraviolet radiation (UVR) is the main risk factor of cSCC, experimental data points toward β-HPVs as co-carcinogens, which appear to be required solely at early stages of skin carcinogenesis by facilitating the accumulation of UVR-induced DNA mutations. Several epidemiological studies relying on different biomarkers of β-HPV infections have also been conducted in immunocompetent individuals to access their association with cSCC development. Additionally, in vivo and in vitro studies are presenting cumulative evidence that E6 and E7 proteins from specific β-HPVs exhibit transforming activities and may collaborate with different environmental factors in promoting carcinogenesis. Nevertheless, further research is crucial to better understand the pathological implications of the broad distribution of these HPVs.
Topics: Humans; Papillomaviridae; Papillomavirus Infections
PubMed: 30673666
DOI: 10.1159/000492659 -
Viruses Aug 2017While the majority of Human papillomavirus (HPV) infections are transient and cleared within a couple of years following exposure, 10-20% of infections persist latently,... (Review)
Review
While the majority of Human papillomavirus (HPV) infections are transient and cleared within a couple of years following exposure, 10-20% of infections persist latently, leading to disease progression and, ultimately, various forms of invasive cancer. Despite the clinical efficiency of recently developed multivalent prophylactic HPV vaccines, these preventive measures are not effective against pre-existing infection. Additionally, considering that the burden associated with HPV is greatest in regions with limited access to preventative vaccination, the development of effective therapies targeting persistent infection remains imperative. This review discusses not only the mechanisms underlying persistent HPV infection, but also the promise of immunomodulatory therapeutic vaccines and small-molecular inhibitors, which aim to augment the host immune response against the viral infection as well as obstruct critical viral-host interactions.
Topics: Antiviral Agents; Female; Humans; Papillomaviridae; Papillomavirus Infections; Papillomavirus Vaccines
PubMed: 28820433
DOI: 10.3390/v9080229 -
Journal of Virology Jul 1991
Review
Topics: Animals; Bovine papillomavirus 1; DNA Replication; Genes, Viral; Humans; Papillomaviridae; Viral Proteins; Viral Structural Proteins; Virus Replication
PubMed: 1645776
DOI: 10.1128/JVI.65.7.3417-3420.1991 -
Uirusu Jun 1998
Review
Topics: Animals; Humans; Oncogene Proteins, Viral; Papillomaviridae; Serologic Tests; Skin Neoplasms; Transformation, Genetic; Virus Replication
PubMed: 9752763
DOI: 10.2222/jsv.48.27 -
Viruses Aug 2015The HPV viral lifecycle is tightly linked to the host cell differentiation, causing difficulty in growing virions in culture. A system that bypasses the need for... (Review)
Review
The HPV viral lifecycle is tightly linked to the host cell differentiation, causing difficulty in growing virions in culture. A system that bypasses the need for differentiating epithelium has allowed for generation of recombinant particles, such as virus-like particles (VLPs), pseudovirions (PsV), and quasivirions (QV). Much of the research looking at the HPV life cycle, infectivity, and structure has been generated utilizing recombinant particles. While recombinant particles have proven to be invaluable, allowing for a rapid progression of the HPV field, there are some significant differences between recombinant particles and native virions and very few comparative studies using native virions to confirm results are done. This review serves to address the conflicting data in the HPV field regarding native virions and recombinant particles.
Topics: Humans; Papillomaviridae; Papillomavirus Infections; Recombination, Genetic; Virion; Virology; Virus Cultivation
PubMed: 26247955
DOI: 10.3390/v7082823 -
Virology Oct 2013The papillomavirus E2 proteins are pivotal to the viral life cycle and have well characterized functions in transcriptional regulation, initiation of DNA replication and... (Review)
Review
The papillomavirus E2 proteins are pivotal to the viral life cycle and have well characterized functions in transcriptional regulation, initiation of DNA replication and partitioning the viral genome. The E2 proteins also function in vegetative DNA replication, post-transcriptional processes and possibly packaging. This review describes structural and functional aspects of the E2 proteins and their binding sites on the viral genome. It is intended to be a reference guide to this viral protein.
Topics: Animals; Base Sequence; Binding Sites; DNA-Binding Proteins; Genome, Viral; Mutation; Oncogene Proteins, Viral; Papillomaviridae; Protein Processing, Post-Translational; Protein Stability; Protein Structure, Tertiary; Transcriptional Activation; Virus Assembly; Virus Replication
PubMed: 23849793
DOI: 10.1016/j.virol.2013.06.006 -
Biological Chemistry Jul 2017Animal and human papillomaviruses (HPVs) replicate persistently in specific types of stratified epithelia of their host. After the initial infection, the viral genome... (Review)
Review
Animal and human papillomaviruses (HPVs) replicate persistently in specific types of stratified epithelia of their host. After the initial infection, the viral genome replicates at low levels in the dividing cells of the epithelium, and these cells form a reservoir of infection that can last for decades. When the infected cells differentiate, viral genomes replicate to high levels to form progeny virus that is released from the surface of the epithelium. This complex life cycle requires several different modes of viral DNA replication, but papillomaviruses are masters at hijacking key cellular processes to facilitate their own reproduction.
Topics: Animals; Genome, Viral; Humans; Papillomaviridae; Viral Proteins; Virus Replication
PubMed: 28315855
DOI: 10.1515/hsz-2017-0113 -
Clinics in Dermatology 1997
Review
Topics: Female Urogenital Diseases; Head and Neck Neoplasms; Humans; Male Urogenital Diseases; Papillomaviridae; Papillomavirus Infections; Serotyping; Skin Diseases, Viral; Tumor Virus Infections
PubMed: 9167904
DOI: 10.1016/s0738-081x(96)00164-2