Phylogenetic Analysis of HPV16 Isolated from Women with Cervical Cancer Based on L2 Gene Partial Sequence in the Province of Dhi-Qar, Iraq

BACKGROUND: As a causative agent for cervical cancer, the human papillomavirus (HPV) is well-recognized. Being a high-risk form, HPV16 is considered and has been confirmed to be associated specifically with cancer of the cervix. AIM: HPV16’s phylogenetic tree and genetic diversity are well known worldwide, but in Iraq, documents on HPV16 genetic diversity among women with cervical cancer are lacking; therefore, the present study focused on phylogenetic analysis of HPV16 isolated cervical cancer based on L2 gene partial sequence. METHODOLOGY: The current study focused on the investigation of HPV16 in women who suffer from cervical cancer. This survey was performed on 93 adult females suffering from cervical cancer during the period from 2017 to 2020. For the molecular study, DNA was extracted and subjected to a polymerase chain reaction (PCR) for detection and amplification of minor capsidprotein L2 gene. Nucleotide sequences of amplified capsid L2 gene were searched using the advanced simple local alignment search tool at GenBank (BLAST). RESULTS: Genetic screening on HPV16 L2 gene by conventional PCR showed that 60 (65%) of cervical cancer cases infected by HPV16 while only 5 (8%) of the healthy control group are positive for HPV16. The results of the NCBI-BLAST homology sequence showed that genetic variation appeared in four strains from five strains of HPV16. CONCLUSION: HPV16 from the main causative factors for cervical cancer with high genetic variation.

[1]  I. Pity,et al.  Human Papillomavirus Genotyping among Different Cervical Smears in Duhok/Iraq , 2019, Asian Pacific journal of cancer prevention : APJCP.

[2]  J. Arbiza,et al.  Analysis of human papillomavirus 16 E6, E7 genes and Long Control Region in cervical samples from Uruguayan women. , 2018, Gene.

[3]  A. Avan,et al.  Genetic susceptibility in cervical cancer: From bench to bedside , 2018, Journal of cellular physiology.

[4]  H. Yoshikawa,et al.  Separate analysis of human papillomavirus E6 and E7 messenger RNAs to predict cervical neoplasia progression , 2018, PloS one.

[5]  C. Meijer,et al.  High Whole-Genome Sequence Diversity of Human Papillomavirus Type 18 Isolates , 2018, Viruses.

[6]  P. Das,et al.  Phylogenetic analysis of Human papillomavirus 16 variants isolated from Indian Breast cancer patients showed difference in genetic diversity with that of cervical cancer isolates. , 2018, Virus research.

[7]  M. Mzibri,et al.  Naturally occurring capsid protein variants L1 of human papillomavirus genotype 16 in Morocco , 2017, Bioinformation.

[8]  Mhairi Marshall,et al.  Defining the genetic susceptibility to cervical neoplasia—A genome-wide association study , 2017, PLoS genetics.

[9]  M. A. Moreira,et al.  Genetic diversity of human papillomavirus types 35, 45 and 58 in cervical cancer in Brazil , 2017, Archives of Virology.

[10]  S. Roychoudhury,et al.  Study of association and molecular analysis of human papillomavirus in breast cancer of Indian patients: Clinical and prognostic implication , 2017, PloS one.

[11]  Qiang Sun,et al.  The Papillomavirus Episteme: a major update to the papillomavirus sequence database , 2016, Nucleic Acids Res..

[12]  O. Shaker,et al.  Human papillomavirus (HPV) in Egyptian females: study by cytology, histopathology, colposcopy and molecular diagnosis of high risk types. , 2016, The Malaysian journal of pathology.

[13]  S. Wilting,et al.  Molecular events leading to HPV-induced high grade neoplasia , 2016, Papillomavirus research.

[14]  G. Trueba,et al.  Prevalence of human papillomavirus types in cervical cancerous and precancerous lesions of Ecuadorian women , 2016, Journal of medical virology.

[15]  Samira Zoa Assoumou,et al.  Sequence variations of human papillomavirus type 16 E6 and E7 genes in cervical cancer isolates from Gabon. , 2015 .

[16]  R. Roden,et al.  L2, the minor capsid protein of papillomavirus. , 2013, Virology.

[17]  Xinan Shi,et al.  Genetic Variability in L1 and L2 Genes of HPV-16 and HPV-58 in Southwest China , 2013, PloS one.

[18]  Chad K. Park,et al.  A Transmembrane Domain and GxxxG Motifs within L2 Are Essential for Papillomavirus Infection , 2012, Journal of Virology.

[19]  K. Ushijima,et al.  Identification of B cell epitopes reactive to human papillomavirus type-16L1- derived peptides , 2012, Virology Journal.

[20]  A. Näsman,et al.  Human Papillomavirus (HPV) 16 E6 Variants in Tonsillar Cancer in Comparison to Those in Cervical Cancer in Stockholm, Sweden , 2012, PloS one.

[21]  A. Spathis,et al.  Genetic Variability and Phylogeny of High Risk HPV Type 16, 18, 31, 33 and 45 L1 Gene in Greek Women , 2011, International journal of molecular sciences.

[22]  A. Rawat,et al.  Identification of Escherichia coli through analysis of 16S rRNA and 16S-23S rRNA internal transcribed spacer region sequences , 2011, Bioinformation.

[23]  S. Franceschi,et al.  Human papillomavirus type distribution in 30,848 invasive cervical cancers worldwide: Variation by geographical region, histological type and year of publication , 2011, International journal of cancer.

[24]  N. Muñoz,et al.  Human papillomavirus genotype attribution in invasive cervical cancer: a retrospective cross-sectional worldwide study. , 2010, The Lancet. Oncology.

[25]  M. Ozbun,et al.  Two Highly Conserved Cysteine Residues in HPV16 L2 Form an Intramolecular Disulfide Bond and Are Critical for Infectivity in Human Keratinocytes , 2009, PloS one.

[26]  R. Roden,et al.  Protection of Rabbits against Challenge with Rabbit Papillomaviruses by Immunization with the N Terminus of Human Papillomavirus Type 16 Minor Capsid Antigen L2 , 2007, Journal of Virology.

[27]  C. R. Martins,et al.  High HPV genetic diversity in women infected with HIV-1 in Brazil , 2006, Archives of Virology.

[28]  E. Unger,et al.  Human Papillomavirus and Cervical Cancer , 2004, Emerging infectious diseases.