| human papillomavirus type 38 isolated from patients with epidermodysplasia verruciformis. | a new type of human papillomavirus (hpv), hpv-38b, was isolated from patients with epidermodysplasia verruciformis and was molecularly cloned. this hpv was shown by hybridization experiments to have almost no sequence homology with other types of reported hpvs, but did show homology with hpv-38, which was recently isolated from a melanoma. a physical map and a rough genetic map of the organization of this hpv are presented. | 1986 | 3032841 |
| high prevalence of a variety of epidermodysplasia verruciformis-associated human papillomaviruses in psoriatic skin of patients treated or not treated with puva. | epidermodysplasia verruciformis-associated human papillomaviruses and in particular human papillomavirus type 5 were recently shown to be highly prevalent in psoriatic skin. we have analyzed lesional skin from 54 psoriasis patients for infections with genital-specific and epidermodysplasia verruciformis-specific human papillomaviruses to define the spectrum of involved human papillomavirus types and to test if it is influenced by psoralen ultraviolet a therapy. using polymerase chain reaction an ... | 1999 | 10417630 |
| human papillomavirus type 38 infection in oral squamous cell carcinomas. | in this study, 53 paraffin-embedded oral squamous cell carcinoma (oscc) biopsy specimens were used. human papillomavirus type 38 (hpv-38) infection was demonstrated in osccs using the pcr technique, dna sequencing analysis, in situ hybridization, and immunohistochemical techniques. additionally, the correlation between hpv-38 infection and expressions of proliferating cell nuclear antigens (pcna) or p53 protein was analyzed immunohistochemically. using consensus primers for the l1 region (l1-pcr ... | 2002 | 12167437 |
| the e6 and e7 proteins of the cutaneous human papillomavirus type 38 display transforming properties. | several studies have suggested the involvement of cutaneous human papillomaviruses (hpvs) in the development of nonmelanoma skin cancers. here we have characterized the in vitro properties of e7 proteins of three cutaneous hpv types, 10, 20, and 38, which are frequently detected in skin specimens. we show that hpv38 e7 is able to inactivate the tumor suppressor prb and induces loss of g(1)/s transition control, a key event in carcinogenesis. in contrast, hpv10 and hpv20 e7 proteins do not displa ... | 2003 | 12525654 |
| p53 mutations are common in human papillomavirus type 38-positive non-melanoma skin cancers. | in cervical cells, the e6 protein of the oncogenic human papillomavirus (hpv) types inactivates p53, promoting its degradation. consequently, mutations of the p53 gene are rarely seen in these cancers. our recent data indicate that the cutaneous hpv38 is involved in skin carcinogenesis. in this study, we have determined the presence of hpv38 and the status of p53 gene in 32 non-melanoma skin cancers. we found that p53 gene is frequently mutated in hpv38-positive skin cancers and that hpv38 e6 do ... | 2004 | 15145527 |
| skin hyperproliferation and susceptibility to chemical carcinogenesis in transgenic mice expressing e6 and e7 of human papillomavirus type 38. | the oncoproteins e6 and e7 of human papillomavirus type 38 (hpv38) display several transforming activities in vitro, including immortalization of primary human keratinocytes. to evaluate the oncogenic activities of the viral proteins in an in vivo model, we generated transgenic mice expressing hpv38 e6 and e7 under the control of the bovine homologue of the human keratin 10 (k10) promoter. two distinct lines of hpv38 e6/e7-expressing transgenic mice that express the viral genes at different leve ... | 2005 | 16282489 |
| skin human papillomavirus type 38 alters p53 functions by accumulation of deltanp73. | the e6 and e7 of the cutaneous human papillomavirus (hpv) type 38 immortalize primary human keratinocytes, an event normally associated with the inactivation of pathways controlled by the tumour suppressor p53. here, we show for the first time that hpv38 alters p53 functions. expression of hpv38 e6 and e7 in human keratinocytes or in the skin of transgenic mice induces stabilization of wild-type p53. this selectively activates the transcription of deltanp73, an isoform of the p53-related protein ... | 2006 | 16397624 |
| subtype hpv38b[fa125] demonstrates heterogeneity of human papillomavirus type 38. | the human papillomaviruses (hpvs) exist as more than 100 distinct types. while variants of hpv are common, only few hpv subtypes have been reported. hpv type 38 has been proposed to be associated with nonmelanoma skin cancer (nmsc), with reported prevalences of up to 55%. a subtype of hpv38 was cloned, completely sequenced and found to have a 96% sequence similarity to prototype hpv38 in the l1 open reading frame. the presence of prototype hpv38 and hpv38b[fa125] was examined in paired biopsies ... | 2006 | 16557595 |
| impairment of the telomere/telomerase system and genomic instability are associated with keratinocyte immortalization induced by the skin human papillomavirus type 38. | the skin human papillomavirus (hpv) types belonging to the genus beta of the hpv phylogenetic tree appear to be associated with nonmelanoma skin cancer. we previously showed that the beta hpv type 38 e6 and e7 oncoproteins are able to inactivate the tumor suppressors p53 and retinoblastoma. here, both viral proteins were expressed in primary human skin keratinocytes in order to study their effects on the telomere/telomerase system. we show that immortalization of skin keratinocytes induced by hp ... | 2008 | 17898088 |
| loss of p53 or p73 in human papillomavirus type 38 e6 and e7 transgenic mice partially restores the uv-activated cell cycle checkpoints. | we have previously shown that human keratinocytes expressing e6 and e7 from the cutaneous human papillomavirus (hpv) type 38 have high levels of a specific form of p53, which in turn activate the transcription of deltanp73 gene. expression of hpv38 e6 and e7 in mouse skin also promotes p53 and deltanp73 accumulation. interestingly, keratinocytes of these mice do not undergo cell cycle arrest after skin ultraviolet (uv) irradiation. here, we provide several lines of evidence that deltanp73 expres ... | 2008 | 18026133 |
| the e6e7 oncoproteins of cutaneous human papillomavirus type 38 interfere with the interferon pathway. | non-melanoma skin cancer is the most frequent malignancy in caucasian populations. evidence suggests the involvement of cutaneous human papillomavirus (hpv) of the genus beta (beta) in this disease. the ability of e6 and e7 of mucosal hpv to promote cellular transformation and inhibit immune response-related pathways plays a key role in cervical carcinogenesis. beta hpv-38 e6 and e7 display transforming activities in in vitro and in vivo models, but their impact on immune surveillance is unknown ... | 2008 | 18519144 |
| atopic dermatitis associated with hpv 38 lower leg verrucosis. | we describe a 45-year-old woman with atopic dermatitis who presented with a progressive, papular eruption over her anterior lower legs that began 30 years earlier. biopsy with polymerase chain reaction analysis revealed lichenified plane warts harboring human papillomavirus 38 dna. no signs or family history of epidermodysplasia verruciformis existed. local trauma from shaving, barrier dysfunction, and decreased cell immunity and interferon production associated with atopic dermatitis are likely ... | 2010 | 20520524 |
| nf-{kappa}b protects human papillomavirus type 38 e6/e7-immortalized human keratinocytes against tumor necrosis factor alpha and uv-mediated apoptosis. | constitutive activation of nf-+¦b signaling is a key event in virus- and non-virus-induced carcinogenesis. we have previously reported that cutaneous human papillomavirus type 38 (hpv38) displays transforming properties in in vitro and in vivo experimental models. however, the involvement of nf-+¦b signaling in hpv38-induced cell growth transformation remains to be determined. in this study, we showed that hpv38 e6 and e7 activate nf-+¦b and that inhibition of the pathway with the i+¦b+¦ superre ... | 2011 | 21715489 |
| cutaneous human papillomavirus type 38 e7 regulates actin cytoskeleton structure for increasing cell proliferation through ck2 and the eukaryotic elongation factor 1a. | we previously reported that the oncoproteins e6 and e7 from cutaneous human papillomavirus type 38 (hpv38) can immortalize primary human keratinocytes in vitro and sensitize transgenic mice to develop skin cancer in vivo. immunofluorescence staining revealed that human keratinocytes immortalized by hpv38 e6 and e7 display fewer actin stress fibers than do control primary keratinocyte cells, raising the possibility of a role of the viral oncoproteins in the remodeling of the actin cytoskeleton. i ... | 2011 | 21697493 |
| combination antiretroviral therapy for hiv in rwandan adults: clinical outcomes and impact on reproductive health up to 24 months. | adult women (n = 113) and men (n = 100) initiating combination antiretroviral therapy (cart) and women not yet eligible for cart (n = 199) in kigali, rwanda, were followed for 6-24 months between 2007 and 2010. in the cart groups, 21% of patients required a drug change due to side effects and 11% of patients had virological failure (defined as >1,000 hiv rna copies/ml) after 12 months of cart. about a third of the pregnancies since hiv diagnosis were unintended. the proportion of women in the pr ... | 2015 | 26257954 |
| downregulation of toll-like receptor 9 expression by beta human papillomavirus 38 and implications for cell cycle control. | innate immunity is the first line of host defense against infections. many oncogenic viruses can deregulate several immune-related pathways to guarantee the persistence of the infection. here, we show that the cutaneous human papillomavirus 38 (hpv38) e6 and e7 oncoproteins suppress the expression of the double-stranded dna sensor toll-like receptor 9 (tlr9) in human foreskin keratinocytes (hfk), a key mediator of the antiviral innate immune host response. in particular, hpv38 e7 induces tlr9 mr ... | 2015 | 26339055 |
| possible human papillomavirus 38 contamination of endometrial cancer rna sequencing samples in the cancer genome atlas database. | viruses are causally associated with a number of human malignancies. in this study, we sought to identify new virus-cancer associations by searching rna sequencing data sets from >2,000 patients, encompassing 21 cancers from the cancer genome atlas (tcga), for the presence of viral sequences. in agreement with previous studies, we found human papillomavirus 16 (hpv16) and hpv18 in oropharyngeal cancer and hepatitis b and c viruses in liver cancer. unexpectedly, however, we found hpv38, a cutaneo ... | 2015 | 26085148 |
| oncoprotein e7 from beta human papillomavirus 38 induces formation of an inhibitory complex for a subset of p53-regulated promoters. | our previous studies on cutaneous beta human papillomavirus 38 (hpv38) e6 and e7 oncoproteins highlighted a novel activity of iκb kinase beta (ikkβ) in the nucleus of human keratinocytes, where it phosphorylates and stabilizes δnp73α, an antagonist of p53/p73 functions. here, we further characterize the role of the ikkβ nuclear form. we show that ikkβ nuclear translocation and δnp73α accumulation are mediated mainly by hpv38 e7 oncoprotein. chromatin immunoprecipitation (chip)/re-chip experiment ... | 2013 | 24006445 |
| human papillomavirus type 38 e6 and e7 act as tumour promoters during chemically induced skin carcinogenesis. | many findings support a possible involvement of a subgroup of human papillomaviruses (hpvs), called cutaneous beta hpv types, in the development of non-melanoma skin cancer. the skin of transgenic (tg) mice expressing viral oncoproteins e6 and e7 from different cutaneous beta hpv types, including hpv38, showed an increased susceptibility to uv-induced and/or chemically induced skin carcinogenesis compared with wild-type animals. in this study, we show that beta hpv38 e6 and e7 oncoproteins act a ... | 2013 | 23223623 |