Phylogenetic Analysis of Human Papillomavirus 16 and 52 L1 Gene from Cervical Cancer in Bandung, Indonesia

Mutia Latief, Ika Agus Rini, Gita Widya Pradini, Gatot Nyarumenteng Adhipurnawan Winarno, Edhyana Sahiratmadja, Herman Susanto

Abstract


BACKGROUND: Chronic infection with high-risk type of human papillomavirus (HPV) can cause cervical cancer. Previous studies showed that multiple infections of HPV are found in cervical cancer caused by multiple HPV infections and the most common are HPV-16 and HPV-52. The origin of HPV-16 circulating in Indonesia varies. The purpose of this study was to explore the origin of multiple infections of HPV-52 and HPV-16 in cervical cancer by using a phylogenetic tree.

METHODS: During July-November 2010, 100 women were diagnosed with cervical cancer in the Department of Obstetrics and Gynecology, Dr. Hasan Sadikin General Hospital, Bandung, Indonesia. Only 96 patients were involved in this study. Ninety-six samples of HPV deoxyribonucleic acid (DNA) were isolated from biopsied tissue of cervical cancer. Multiple infections of HPV genotypes HPV-16 and HPV-52 were confirmed by using the linear assay for HPV genotyping test. Afterward,HPV-52L1 gene was amplified by using self-designed primer. L1 gene was also sequenced and analyzed using phylogenetic program (MEGA6.06).

RESULTS: The result of phylogenetic tree construction showed that isolated HPV-52 originated from multiple infections of HPV-16 and HPV-52 from cervical cancer patients in Bandung were in a subgroup with isolates originating from EU077219 Canada (America) and KT799980 southwest China (Asia). Isolate HPV-16 in one subgroup with isolates originating from KU951191.1 (Southwest China).

CONCLUSION: L1 gene sequence from multiple infections isolated from HPV-16 and HPV-52 from cervical cancer patients in Bandung refers to the variation of L1 gene reported from Canada and southwest China. This proves that Indonesia’s HPV clusters are located in the strains found in America and Asia.

KEYWORDS: multiple infections, HPV-16, HPV-52, L1 gene, phylogenetic


Full Text:

PDF

References


Ferlay J, Soerjomataram I, Dikshit R, Eser S, Mathers C, Rebelo M, et al. Cancer incidence and mortality worldwide: Sources, methods and major patterns in GLOBOCAN 2012. Int J Cancer. 2015; 136: E359-86, CrossRef.

Catarino R, Petignat P, Dongui G, Vassilakos P. Cervical cancer screening in developing countries at a crossroad: Emerging technologies and policy choices. World J Clin Oncol. 2015; 6: 281-90, CrossRef.

Vet JNI, de Boer MA , Van den Akker BEWM, Siregar B, Lisnawati, Budiningsih S, et al. Prevalence of human papillomavirus in Indonesia: a population-based study in three regions. Br J Cancer. 2008; 99: 214-8, CrossRef.

Bruni L, Barrionuevo RL, Albero G, Aldea M, Serrano B, Valencia S, et al. Human papillomavirus and related diseases in Indonesia. ICO Information Center on HPV and Cancer. 2015; 23: 74.

Bzhalava D, Guan P, Franceschi S, Dillner J, Clifford G. A systematic review of the prevalence of mucosal and cutaneous human papillomavirus types. J Virol. 2013; 445: 224-31, CrossRef.

Thomsen LT, Frederiksen K, Christian M, Junge J, Castle PE, Iftner T, et al. High-risk and low-risk human papillomavirus and the absolute risk of cervical intraepithelial neoplasia or cancer. J Obst and Gynecol. 2014; 123: 57-64, CrossRef.

International Agency for Research and Cancer. IARC Monograph Biological Agents: Volume 100B A Review of Human Carcinogens. Lyon: International Agency for Research and Cancer; 2012, article.

Bernard HU, Burk RD, Chen Z, Van Doorslaer K, Hausen H zur, de Villiers EM. Classification of papillomaviruses (PVs) based on 189 PV types and proposal of taxonomic amendments. J Virol. 2010; 401: 70-9, CrossRef.

Tobing MDL, Sahiratmadja E, Dinda M, Hernowo BS, Susanto H. Human papillomavirus genotypes profile in cervical cancer patient at Dr. Hasan Sadikin General Hospital, Bandung Indonesia. Asian Pac J Cancer Prev. 2014; 15: 5781-5, CrossRef.

Sahiratmadja E, Tobing MDL, Dewayani BM, Hernowo BS, Susanto H. Multiple human papilloma virus infections predominant in squamous cell cervical carcinoma in Bandung. Univ Med. 2014; 33: 58-64, CrossRef.

Hall BG. Building phylogenetic trees from molecular data with MEGA. J Mol Biol Evol. 2013; 30: 1229-35, CrossRef.

Burk RD, Chen Z, Van Doorslaer K. Human papillomaviruses: Genetic basis of carcinogenicity. Public Health Genomics. 2009; 12: 281-90, CrossRef.

Chen Q, Luo Z, Lin M, Yang L, Yang L, Ju G. Evaluation of the genetic variability of human papillomavirus type 52. Int J Mol Med. 2012; 30: 535-44, CrossRef.

Fadhilah FR, Sahiratmadja E, Safitri R, Maskoen AM, Susanto H. Analisis filogenetik gen L1 human papillomavirus 16 pada penderita kanker serviks di Bandung. MKB. 2015; 47: 174-8, CrossRef.

Suhandono S, Kencana UDA, Kristianti T, Sahiratmadja E, Susanto H. Cloning, expression and bioinformatic analysis of human papillomavirus type 52 L1 capsid gene from Indonesian patient. Microbiol Indones. 2014; 8: 94-102, CrossRef.

Kantathavorn N, Mahidol C, Sritana N, Sricharunrat T, Phoolcharoen N, Auewarakul, et al. Genotypic distribution of human papillomavirus (HPV) and cervical cytology findings in 5906 Thai women undergoing cervical cancer screening programs. Inf Agents and Cancer. 2015; 10: 7, CrossRef.

Baloch Z, Yasmeen N, Li Y, Ma K, Wu X, Yang S, et al. Prevalence and risk factors for human papillomavirus infection among Chinese ethnic women in southern of Yunnan, China. Braz J Infect Dis. 2017; 21: 325-32, CrossRef.




DOI: https://doi.org/10.18585/inabj.v10i1.296

Indexed by:

                 

                

                

  

 

The Prodia Education and Research Institute