Dataset Information

Detecting Human Papillomavirus Type 16 in Cervical Cancer Patients with Molecular Variation of Gene L1 in Riau Province Indonesia.

ABSTRACT:

Background

Cervical cancer is the second most deadly cancer in the world after breast cancer. The cancer is caused by infection of high risk Human Papillomavirus (HPV) type 16. It is often found in cervical cancer of which the genome structure is composed of L1 proteins. The L1 protein makes up the viral capsid that has an important role in causing the cervical epithelium. Several studies have found the differences in HPV nucleotides variants that lead to changes in amino acids that disrupt the structure, the natural function of the virus itself, and ultimately lead to changes in biological functions including host immunological recognition. Variation of the L1 gene also affects the effectiveness of existing vaccines.

Methods

This research was a descriptive study conducted at the laboratory of microbiology, the Faculty of Medicine, Universitas Riau, Pekanbaru from February to August 2018. The study was aimed at looking at the molecular variations of the L1 HPV type 16 gene and examining phylogenic kinship.

Results

The SNPs (Single Nucleotide Polymorphism) which occurred in 26 sample isolates are the substitution of C/G (6240), A/G (6432), T/G (6686), C/T (6824). These variations also cause changes in amino acids, insertion of ATC nucleotide bases (6902), and deletions of GAT bases (6954).

Conclusion

There are molecular variations of the L1 HPV type 16 gene which can cause different host immune responses. Phylogenic kinship of HPV type 16 isolate in Riau is similar to Asian-American isolate.

SUBMITTER: Savira M

PROVIDER: S-EPMC9258658 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundThe variation of human papillomavirus (HPV) genes or HPV variants demonstrates different risks of cervical cancer. Mutation in the long control region (LCR) at YY1-motifs is one of the mechanisms for enhancing viral oncogene expression during the course of cancer cell progression. In Thai women, cervical cancers are almost always associated with HPV16 variant sub-lineage Asian (HPV16As); however, the mechanism involved remains elusive. The aim of this study was to understand further the oncogenic potential of HPV16As.MethodsA total of 82 HPV16-positive specimens from Thai women were selected from formalin-fixed paraffin-embedded cervical tissues, and the full length E6 gene of each specimen was amplified and sequenced. LCRs of the HPV16As-positive cases were amplified and sequenced to analyze their polymorphisms. Transcriptional activities of the HPV16As LCRs were then compared with sub-lineage European (EUR), sub-lineage Asian-American 1 (AA1) and HPV16 prototype by insertion of the LCRs into the pGL3-Basic vector.ResultsThe HPV16 DNA sequences were classified as HPV16 prototype (18.3%), Asian (As, 61%), Asian American-1 (AA1, 8.5%), European (EUR, 7.3%), Asian African-2 (AFR2, 3.7%) and Java-135C (J135C, 1.2%). The prevalence of HPV16As was 30% in low-grade squamous intraepithelial lesion (LSIL), while that in high-grade squamous intraepithelial lesion (HSIL) and squamous cell cervical carcinoma (SCC) were 63.9% and 66.7%, respectively, which demonstrates a significant association of HPV16As with the disease severity. LCR polymorphisms from 43 HPV16As positive cases were analyzed by PCR-sequencing. Thirty-eight nucleotide variation positions spanned nucleotide positions 7157-82. Ten new mutations found in the HPV16As LCRs were located predominantly at the enhancer and proximal to the 3'-end of the early promoter. The LCRs of the common HPV16As, EUR and AA1 showed 5, 13 and 23-fold higher activity than the HPV16 prototype LCR, while those of the new nucleotide variations of As showed 19 (As-sv1) and 30 (As-sv14) -fold higher activity than the HPV16 prototype.ConclusionsHPV16As DNA sequence variation, especially at the proximal to early promoter in the LCR, enhances transcriptional activity. This could be one of the possible mechanisms for HPV16As-associated cervical cancer development.