Polymorphism in the E6 gene of human papillomavirus type 16 in the cervical tissues of Korean women

Bae

J of Obstet and Gynaecol

et al. 2011

Section: Discussioncontrasting

confidence: 69%

Distribution of human papillomavirus type 16 E6 and E7 gene variants in the progression of cervical dysplasia in Korean women

Bae

J of Obstet and Gynaecol

et al. 2011

Journal of General Virology

“…Dashes indicate no variation. As ---C ------E378D 1 0?76 As -------G --K382E 1 0?76 A f 1 ---------a 1 0 ?76 AA/Af2 ----C ----a T379P 1 0?76 n 1 1 1 1 1 2 1 1 1 2 1 3 1 in Korean women (Kang et al, 2005). A previous report showed that other variations in E6 (E/G131T) result in amino acid changes in potential T-cell receptor-or HLAbinding regions (Ellis et al, 1995).…”

Section: Discussionmentioning

confidence: 98%

Analysis of mutations in the E6/E7 oncogenes and L1 gene of human papillomavirus 16 cervical cancer isolates from China

Chen

et al. 2006

Human papillomavirus type 16 (HPV16) has a number of intratypic variants; each has a different geographical distribution and some are associated with enhanced oncogenic potential. Cervical samples were collected from 223 cervical cancer patients and from 196 age-matched control subjects in China. DNA samples were amplified by using primers specific for the E6, E7 and partial L1 regions. Products were sequenced and analysed. It was found by using a PCR-sequence-based typing method that HPV infection rates in China were 92?8 % in cervical cancer patients and 15?8 % in healthy controls. HPV16 was detected in 70?4 % of cervical cancer patients and in 6?1 % of controls. In HPV16-positive cervical cancers, 23?6 % belonged to the prototype, 65?5 % were of the Asian variant, 5?5 % were of African type 1 and 3?6 % were European variants, whilst only one was a new variant that differed from any variant published so far. Prevalences of HPV16 E6 D25E and E113D variants were 67?3 and 9 %, respectively. In addition to D25E and E113D, the following E6 variations were found in this study: R129K, E89Q, S138C, H78Y, L83V and F69L. The results also showed that the prevalences of three hot spots of E7 nucleotide variation, N29S, S63F and a silent variation, nt T846C, were 70?2 % (33/47), 51?1 % (24/47) and 61?7 % (29/47), respectively. The following L1 variations were found in this study: S377A, K387E, E378D, K382E and T379P. It was also found that the average age of Asian variant-positive cervical cancer patients (42?98±10?43 years) was 7?56 years lower than that of prototype-positive patients (50?54±10?91). It is suggested that the high frequency of HPV16 Asian variants might contribute to the high incidence of cervical cancer in China. INTRODUCTIONHuman papillomavirus (HPV) infection is the central cause of cervical cancer (Muñoz, 2000). It has been coevolving with its natural hosts for several million years (Ho et al., 1991). This DNA virus acts by the expression of two viral oncoproteins, E6 and E7. However, not all cervical infections with oncogenic HPV types will progress to cervical cancer. Factors that are described to be important in the risk of progression to cancer are of both host and viral origin. One viral factor is the type/subtype of the papillomavirus involved. Almost 30 distinct types of HPV, both oncogenic and non-oncogenic, have been described to infect the genital tract. Our previous study showed, by using hybrid capture 2, that high-risk HPV prevalence was 89?9 % (427/475) in invasive cervical cancer (ICC) (Wu et al., 2006a). The most common HPV DNA type found in cervical cancers among Chinese women was HPV16 (79?6 %), followed by HPV58 (5?92 %) and HPV33 (3?29 %) (Wu et al., 2006a). Other research reports that HPV16 is the most common, being associated with >50 % of cervical cancers (Muñoz, 2000). HPV16 variants are described in phylogenetic branches, the distribution of which varies geographically. The prototype described by Seedorf et al. (1985) is a German isolate and a member of the European (E) branch....

“…This variant leads to an amino acid change at residue 83 from a leucine to a valine (denoted L83V) and may increase the pathogenicity of HPV16 by enhancing persistency of infection in cervical cancer, 29,30 although the results are still controversial. [31][32][33] In HNSCC, T350G is the most prevalent E6 genomic variant and has a higher viral load compared with the prototype. 34,35 In contrast, the E7 genetic sequence is widely conserved in cervical cancer, as demonstrated in a cohort of 5570 HPV16infected cases.…”

Section: The True Impact Of Hpv On Head and Neck Cancer Hpv Infectionmentioning

confidence: 99%

Human papillomavirus as a driver of head and neck cancers

2019

The human papillomavirus (HPV) family includes more than 170 different types of virus that infect stratified epithelium. High-risk HPV is well established as the primary cause of cervical cancer, but in recent years, a clear role for this virus in other malignancies is also emerging. Indeed, HPV plays a pathogenic role in a subset of head and neck cancers-mostly cancers of the oropharynx-with distinct epidemiological, clinical and molecular characteristics compared with head and neck cancers not caused by HPV. This review summarises our current understanding of HPV in these cancers, specifically detailing HPV infection in head and neck cancers within different racial/ethnic subpopulations, and the differences in various aspects of these diseases between women and men. Finally, we provide an outlook for this disease, in terms of clinical management, and consider the issues of 'diagnostic biomarkers' and targeted therapies.