Primer-Directed Sequencing of Human Papillomavirus Types

Delius, Hajo; Hofmann, Birgit

doi:10.1007/978-3-642-78487-3_2

Cited by 75 publications

(53 citation statements)

References 62 publications

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“…Calleja-Macias et al 19 in 2005 resequenced the original HPV 52 reference isolate (accession no. X74481) 27 and confirmed the omission of the five-basepair segment at the genomic positions 7,387-7,391. The corrected sequence was used as the HPV52 reference sequence.…”

Section: Pcr Amplificationmentioning

confidence: 54%

Unique variants of human papillomavirus genotypes 52 and 58 and risk of cervical neoplasia

Chang

Chen

Lee³

et al. 2010

Intl Journal of Cancer

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Human papillomavirus (HPV) 52 and 58 are oncogenic HPV types prevalent in Asia. Our study aims to explore intratypic variants of HPV 52 and 58 in Taiwan. A total of 11,923 women were enrolled from seven townships in [1991][1992]. HPV DNA in their cervical cells was detected and typed by EasyChip V R HPV blot. Among 424 participants infected with HPV 52 and/or 58, nucleotide variations were determined in cervical cell samples of 406 participants by the polymerase chain reaction sequencing of the long control region, E6 and E7 genes. Nonprototype-like variants including lineages B and C were detected in 278 (99.3%) of 280 HPV 52 samples. The prototype and prototype-like group (lineage A) of HPV58 was found in 132 (98.5%) of 134 HPV 58 samples, with sublineage A1, A2 and A3 variant in 14.2, 27.6 and 56.7%, respectively. Among women infected with single HPV 52 type, the C variant (vs. B variant) was associated with an increased prevalence of cytologically diagnosed high-grade squamous intraepithelial lesion or worse lesions showing an age-adjusted odds ratio (95% confidence interval, CI) of 5.2 (1.0-27.6) and an increased prevalence of histologically confirmed high-grade cervical intraepithelial neoplasia or more severe lesions with an age-adjusted odds ratio (95% CI) of 7.6 (1.3-43.8). It was concluded that frequency distributions of HPV 52 and 58 variants in Taiwan were different from those in European and American populations. The association between C variant of HPV 52 and prevalence of cervical neoplasia needs further validation.Oncogenic human papillomavirus (HPV) is the major cause of cervical cancer. In addition to HPV 16 and 18, HPV 52 and 58 are also considered high-risk types for cervical intraepithelial lesions (CINs) and invasive carcinoma. 1,2 The unusually high prevalence of HPV 52 and 58 has been reported in Chinese populations living in China 3,4 and Taiwan. [5][6][7][8] In a previous report of our study, the prevalence of high-grade squamous intraepithelial lesion (HSIL) or worse lesions among participants with single-type infection of HPV 16, HPV 58 and HPV 52 at study entry was 31.9, 35.7 and 13.3%, respectively. 9 The participants infected with HPV 16, HPV 58 or HPV 52 had an increased prevalence of cervical cancer and carcinoma in situ (CIS).Intratypic HPV variants are characterized by the difference of less than 2% in nucleotide sequence from the prototypic L1 gene. 10 The genetic divergence among variants can differ by as much as 5% in the noncoding long control region (LCR). 11 But a study based on the complete genome analyses of HPV 16 showed that the E5-L2 intergenic region and the E4 and E5 genes are also hypervariable. 12 In a recent study, HPV variants can be classified based on their nucleotide sequence differences with most variants differing by <3%; type-specific variant lineages are defined based on a complete genome nucleotide sequence having >1% dissimilarity with the prototype and are named according to the phylogenetic tree topologies for each individual type. 13 Previous studie...

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Section: Pcr Amplificationmentioning

confidence: 54%

Unique variants of human papillomavirus genotypes 52 and 58 and risk of cervical neoplasia

Chang

Chen

Lee³

et al. 2010

Intl Journal of Cancer

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“…Each plasmid was directly sequenced, first with primers selected from the vector sequence and later with additional primers designed from sequence walking (Delius & Hofmann, 1994). Sequencing was performed in the Einstein DNA sequencing core facility, and the overlapped sequences were assembled manually.…”

Section: Methodsmentioning

confidence: 99%

Lack of the canonical pRB-binding domain in the E7 ORF of artiodactyl papillomaviruses is associated with the development of fibropapillomas

Narechania

Terai

Chen

et al. 2004

Journal of General Virology

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The L-X-C-X-E pRB-binding motif of papillomavirus (PV) E7 proteins has been implicated in the immortalization and transformation of the host cell. However, sequencing of the complete genomes of bovine papillomavirus type 3 (BPV-3), bovine papillomavirus type 5 (BPV-5), equine papillomavirus (EQPV) and reindeer (Rangifer tarandus) papillomavirus (RPV) supports the notion that the pRB-binding motif is not ubiquitous among E7 proteins in the PV proteome. Key among the animal groups that lack the pRB-binding domain are the artiodactyl PVs, including European elk PV (EEPV), deer PV (DPV), reindeer PV (RPV), ovine PVs types 1 and 2 (OvPV-1 and -2) and bovine PVs 1, 2 and 5 (BPV-1, -2 and -5). Whereas the presence of the pRB-binding domain is normally associated with papillomas, the artiodactyl PVs are marked by the development of fibropapillomas on infection. Previous studies emphasized the role of E5 in the pathogenic mechanism of fibropapilloma development, but correlation between the lack of an E7 pRB-binding domain and the unique pathology of the artiodactyl PVs suggests a more complicated mechanism and an early evolutionary divergence from a pRB-binding ancestor. INTRODUCTIONPapillomaviruses (PVs) are highly species-specific pathogens. They form a heterogeneous group of closed-circular, double-stranded DNA viruses measuring about 8 kb in size (Sundberg et al., 1996). Most PVs target the basal cells of dermal or mucosal epithelia (Cheville & Olson, 1964), and infection has been implicated in both benign and malignant lesions of epithelia in a broad range of animals (Sundberg & O'Banion, 1989). Though almost all known human PVs (HPVs) infect dermal or mucosal surfaces, in some animal PVs, most notably in the artiodactyl ruminant PVs, fibroblasts appear to be the primary target cells (Sundberg et al., 1985). However, regardless of species, infection generally manifests as a papilloma or fibropapilloma, and follows a cytopathic mechanism of cell proliferation (Sundberg et al., 1996). Historically, PVs had been classified according to their tissue tropism, and this grouping was supported by later phylogenetic analysis of PV sequence data (Chan et al., 1995;de Villiers, 2001;Myers, 1994). PV phylogenies typically subdivide into mucosal/genital HPVs, cutaneous EV HPVs and three main animal PV clades: the artiodactyl ruminant PVs, the distant avian PV group and a group containing canine, feline, rabbit and rodent PV types. However, sequence analysis has highlighted some significant exceptions. BPV-3, BPV-4 and BPV-6 do not group with the artiodactyl PVs, but instead form an isolated taxon (Jarrett et al., 1984), and HPV-1, HPV-41 and HPV-63 are most closely related to the canine and feline PVs, sharing little similarity to HPVs in either the mucosal or the cutaneous groups (Egawa et al., 1993).Although most work in the area has focused on HPVs, an ever-increasing number of animal PV isolates have been sequenced. These animal PVs share key clinical features of GenBank data deposited: bovine papillomavirus 3, AF486184; bo...

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“…The fragments were inserted into pUC18 and transformed into E. coli DH5α. The longer fragments were sequenced using the primer walking strategy which has been described in detail by Delius & Hofmann (1994). All oligonucleotides used for PCR amplification or sequencing were purchased from Eurogentec.…”

Section: Methodsmentioning

confidence: 99%

“…All samples were electrophoresed in 1 % agarose, denatured and transferred by vacuum to a nylon membrane (Hybond-N ; Amersham) in an alkaline buffer. Thirty ng of the I2 PCR product was labelled with [α-$#P]dATP using the Gibco Random Primers DNA Labelling system and this served as a homologous Fuchs et al (1986) and Delius & Hofmann (1994), respectively. probe.…”

Section: Methodsmentioning

confidence: 99%

Detection of new human papillomavirus sequences in skin lesions of a renal transplant recipient and characterization of one complete genome related to epidermodysplasia verruciformis-associated types.

Bens

Wieland

Hofmann

et al. 1998

Journal of General Virology

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Human papillomavirus (HPV) DNA, originally isolated from patients suffering from the skin disease epidermodysplasia verruciformis (EV), and a growing number of related sequences have recently been detected in a high percentage of benign and malignant skin lesions of both immunosuppressed and immunocompetent people. HPV L1 DNA fragments (374-389 bp long) from a solar keratosis and a squamous cell carcinoma (SCC) of a renal transplant recipient were amplified, cloned and sequenced. In 54 clones, six different HPV sequences were identified. One of these six corresponded to the known type HPV-8 and two (RTRX3 and RTRX7) have been described previously in cutaneous lesions of immunosuppressed patients. The remaining three sequences were different from all known HPV types : an HPV-9-related sequence (77n4 % identity), an RTRX2-related sequence

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Primer-Directed Sequencing of Human Papillomavirus Types

Cited by 75 publications

References 62 publications

Unique variants of human papillomavirus genotypes 52 and 58 and risk of cervical neoplasia

Unique variants of human papillomavirus genotypes 52 and 58 and risk of cervical neoplasia

Lack of the canonical pRB-binding domain in the E7 ORF of artiodactyl papillomaviruses is associated with the development of fibropapillomas

Detection of new human papillomavirus sequences in skin lesions of a renal transplant recipient and characterization of one complete genome related to epidermodysplasia verruciformis-associated types.

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