Nucleotide sequence of human papillomavirus type 31: A cervical neoplasia-associated virus

Goldsborough, Mindy D.; DiSilvestre, Debbie; Temple, Gary F.; Lörincz, Attila T.

doi:10.1016/0042-6822(89)90545-x

Cited by 101 publications

(65 citation statements)

References 31 publications

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“…Fragments of GP-PCR from these lines were, therefore, directly subjected to sequence analysis and the nucleotide sequences of the 2 samples were compared with cumulative data within the GenBank database (data not shown). SNU-682 showed 100% homology to reported HPV-33 (Cole and Streeck, 1986) in the nt 6589-6702 spectrum and SNU-778 showed 99% homology to reported HPV-31 (Goldsborough et al, 1989) in the nt 6550-6652 spectrum. SNU-778 harbored only single nucleotide change (G to T) at nt 6586.…”

Section: Typing Of Hpv Dnamentioning

confidence: 87%

Establishment and characterization of 12 uterine cervical-carcinoma cell lines: Common sequence variation in theE7 gene of HPV-16-positive cell lines

Kim

Park

et al. 1997

Int. J. Cancer

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Carcinoma of the uterine cervix is one of the most common neoplasms in women, and about 90% of all cervical carcinomas are epidemiologically associated with infection by high-risk human papillomaviruses (HPV) such as types 16, 18, 31 and 33 (Zur Hausen, 1991).Because most available cervical-cancer cell lines were initiated more than 20 years ago (Spence et al., 1988), they have been extensively passaged in culture for hundreds of times in uncontrolled growth conditions, and this might have resulted in changes in the original characteristics of the primary tumor (Spence et al., 1988;Braun et al., 1993). Moreover, because establishment is difficult, the numbers of recently established cell lines with a low passage number are limited (Spence et al., 1988;Braun et al., 1993). The establishment from histopathologically varied primary tumors of cervical-cancer cell lines with a low passage number and an understanding of their characteristics are therefore required.In cervical cancers, a high-risk viral DNA genome is often found to be integrated into the host chromosome by common disruption of the viral E1/E2 region (Schwarz et al., 1985;Chen et al., 1994). In in vitro experiments, E2 repress transcription from the promoters of the E6 and E7 genes. In contrast, E6/E7 genes are actively transcribed in E2-deleted cervical cancers and cell lines (Schwarz et al., 1985).E6 and E7 proteins have been shown to form complexes with the normal cellular protein, p53, or the retinoblastoma-susceptibility gene product, pRb, both of which are well-known tumor suppressors, and those complexes lead to inactivation of the suppression function . Oncogenic HPV-type E6 protein specifically binds to wild-type p53 protein and subsequently enhances the degradation of p53 protein in an ATP/ubiquitin-dependent manner (Scheffner et al., 1990). In addition, pRb is inactivated by binding with E7 protein or through mutation. E7 protein of high-risk HPVs complex with pRb to inactivate the tumor-suppressor function of pRb (reviewed by McIntyre et al., 1993). Functional relevance of alterations at the Rb-binding domain in the E7 gene remains unclear.In this context, we established 12 new uterine cervical-cancer cell lines (SNU-17, SNU-487, SNU-523, SNU-682, SNU-703, SNU-778, SNU-902, SNU-1000, SNU-1005, SNU-1160, SNU-1245 and SNU-1299) with early passages and described cell phenotypes, including histopathology of the primary tumor and in vitro growth characteristics. We also performed molecular characterization, including DNA-fingerprinting analysis and HPV detection, typing and determination of physical form (integrated or episomal) of viral DNA. RNA expression of HPV E6/E7 viral transcripts, sequence variation in the E7 gene of HPV and genetic alteration of p53 were also examined. MATERIAL AND METHODS Cell-line establishment and maintenanceCell lines were established from pathologically proven uterine cervical carcinomas (Table I). Solid tumors were finely minced with scissors and dissociated into small aggregates by pipetting. Appropriate amounts...

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Section: Typing Of Hpv Dnamentioning

confidence: 87%

Establishment and characterization of 12 uterine cervical-carcinoma cell lines: Common sequence variation in theE7 gene of HPV-16-positive cell lines

Kim

Park

et al. 1997

Int. J. Cancer

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“…A viral isolate was defined as a distinct variant if one or more nucleotide alterations (relative to the prototype 25 and other isolates) were detected in the region analyzed. An analysis of the 1,000-bp fragments on 533 samples revealed a total of 77 variants.…”

Section: Characterization Of Hpv31 Variantsmentioning

confidence: 99%

Association of human papillomavirus type 31 variants with risk of cervical intraepithelial neoplasia grades 2–3

Schiffman

Koutsky

et al. 2012

Intl Journal of Cancer

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Although the lineages of human papillomavirus type 31 (HPV31) variants are recognized, their clinical relevance is unknown. The purpose of our study was to examine risk of cervical intraepithelial neoplasia Grades 2-3 (CIN2/3) by HPV31 variants. Study subjects were women who participated in the atypical squamous cells of undetermined significance and low-grade squamous intraepithelial lesion Triage Study and who had HPV31 infections detected at one or more visits. They were followed semi-annually over 2 years for detection of HPV DNA and cervical lesion. HPV31 isolates were characterized by DNA sequencing and assigned into 1 of 3 variant lineages. CIN2/3 was histologically confirmed in 127 (27.0%) of the 470 HPV31-positive women, 83 diagnosed at the first HPV31-positive visit and 44 thereafter. The odds ratio for the association of 2-year cumulative risk of CIN2/3 was 1.7 (95% CI: 1.0-2.9) for infections with A variants and 2.2 (95% CI: 1.2-3.9) for infections with B variants as compared to those with C variants. Among women without CIN2/3 at the first HPV31-positive visit, the risk of subsequent CIN2/3 was 2.2-fold greater for those with A variants (95% CI: 1.0-4.8) and 2.0-fold greater for those with B variants (95% CI: 0.9-4.9) as compared to those with C variants. Similar associations were observed when CIN3 was used as the endpoint. The findings from our study help to tag HPV31 variants that differ in risk of CIN2/3 and to explain in part why some HPV31 infections regress spontaneously and others lead to disease progression.Cervical infection with human papillomavirus (HPV) types is a necessary cause of cervical cancer and its precursor, cervical intraepithelial neoplasia Grades 2-3 (CIN2/3). 1-3 To date, >150 papillomavirus types have been fully characterized and classified, from the higher to lower taxon, as genera, species and type. 4,5 HPV types are known to differ in their tropisms and oncogenic potentials. Studies of the intratypic variation, i.e., the variant, a level below the taxon of type, have focused mainly on HPV16 and HPV18, showing that some variants were more aggressive than others. [6][7][8][9][10][11][12] HPV31 is one of the oncogenic types, most closely related to HPV16. Prevalence of some HPV types may vary geographically. Results from a recent meta-analysis (including 215 studies worldwide) have shown that on average prevalence of HPV31 infection ranks fourth, after types 16, 18 and 45, in cases of cervical cancer and second, only after type 16, in women with high-grade squamous intraepithelial lesion (referring both to cytologically detected high-grade lesions and histologically diagnosed CIN2/3 or carcinoma in situ in this analysis). 1 Clinical relevance of HPV31 variants has been rarely described, 13-15 although the intratypic variations in the L1, E6, E7 and long control region were recognized. 14-21 A recent study by Chen et al. 22 has defined HPV31 variants as A, B and C lineages based on the whole genome analyses. This provides a basis to view the variant as a distinct phylogenet...

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“…HPV57 DNA was originally described as HPV2 (23). The HPV8 (28), HPV31 (29,30), COPV (31), and ROPV (32) genomes were obtained from T. Iftner (University of Tübingen, Tübingen, Germany), L. Laimins (Northwestern University, Chicago), R. Schlegel (Georgetown University, Washington, DC), and N. Christensen (Pennsylvania State University, Hershey, PA), respectively. Recircularization of HPV1a, HPV4, HPV31, HPV57, and DPV genomes was necessary because they were cloned in the E2 gene.…”

Section: Methodsmentioning

confidence: 99%

Variations in the association of papillomavirus E2 proteins with mitotic chromosomes

Oliveira

Colf

McBride

2006

Proc. Natl. Acad. Sci. U.S.A.

101

145

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The E2 protein segregates episomal bovine papillomavirus (BPV) genomes to daughter cells by tethering them to mitotic chromosomes, thus ensuring equal distribution and retention of viral DNA. To date, only the BPV1 E2 protein has been shown to bind to mitotic chromosomes. We assessed the localization of 13 different animal and human E2 proteins from seven papillomavirus genera, and we show that most of them are stably bound to chromosomes throughout mitosis. Furthermore, in contrast to the random association of BPV1 E2 with mitotic chromosomes, several of these proteins appear to bind to more specific regions of mitotic chromosomes. Using human papillomavirus (HPV) type 8 E2, we show that this region is adjacent to centromeres͞kinetochores. Therefore, E2 proteins from both HPV and animal papillomavirus bind to mitotic chromosomes, and there are variations in the specificity of this binding. Only the ␣-papillomavirus E2 proteins do not stably associate with mitotic chromatin throughout mitosis. These proteins closely associate with prophase chromosomes and bind to chromosomes in telophase but not in metaphase. However, extraction of mitotic cells before fixation results in ␣-E2 proteins binding to the pericentromeric region of metaphase chromosomes, as observed for HPV8 E2. We postulate that this is the authentic target of these E2 proteins but that additional factors or a specialized cellular environment is required to stabilize this association. Thus, E2-mediated tethering of viral genomes to mitotic chromosomes is a common strategy of papillomaviruses, but different viruses have evolved different variations of this theme.human papillomavirus ͉ mitosis ͉ replication ͉ segregation T here are 17 distinct genera of Papillomaviridae (1); each virus infects a specific region of cutaneous or mucosal epithelium in a particular host. For example, human papillomavirus (HPV) types 1, 2, 3, and 4 cause plantar and palmar warts whereas HPV5 and HPV8 are found in cutaneous lesions of epidermodysplasia verruciformis. Mucosal HPV types such as HPV6, HPV11, HPV16, and HPV31 infect genital and sometimes oral epithelia. These infections are usually persistent, and so papillomaviruses need a mechanism to efficiently retain the extrachromosomal genomes within dividing cells.The viral E1 and E2 proteins initiate viral DNA replication by binding to the replication origin. Multiple E2 binding sites are required in addition for the genome to be stably maintained in dividing cells (2). The bovine papillomavirus (BPV) type 1 E2 protein tethers the genomes by means of the E2 binding sites to cellular mitotic chromosomes (3-5) to ensure that they are retained in the nucleus and distributed to daughter cells. This mechanism is a common one in persistent episomal viruses; Epstein-Barr virus and human herpesvirus 8 also each encode a protein that tethers the viral genomes to mitotic chromosomes to ensure their faithful segregation.The E2 protein is also a transcriptional regulator, consisting of a transactivation domain and a dimerization͞DN...

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Nucleotide sequence of human papillomavirus type 31: A cervical neoplasia-associated virus

Cited by 101 publications

References 31 publications

Establishment and characterization of 12 uterine cervical-carcinoma cell lines: Common sequence variation in theE7 gene of HPV-16-positive cell lines

Establishment and characterization of 12 uterine cervical-carcinoma cell lines: Common sequence variation in theE7 gene of HPV-16-positive cell lines

Association of human papillomavirus type 31 variants with risk of cervical intraepithelial neoplasia grades 2–3

Variations in the association of papillomavirus E2 proteins with mitotic chromosomes

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