Evaluation of human papillomavirus 16 and human papillomavirus 18 in saliva of chronic smokers in Malaysian population: An In vitro observational study

• Main Authors: E V Soma Sekhar Goud, Shanthi Malleedi, Anand Ramanathan, Gou Rean Wong, Elin Mong Theng Wei, Yvonne Tan Yi Wen, Lee Yoke Hin Yeung, Lee Cheun Wai
• Format: Article
• Language: English
• Published: Wolters Kluwer Medknow Publications 2017-01-01
• Series: Archives of Medicine and Health Sciences
• Subjects: Carcinoma; human papillomavirus; real-time polymerase chain reaction; saliva; smoking
• Online Access: http://www.amhsjournal.org/article.asp?issn=2321-4848;year=2017;volume=5;issue=1;spage=16;epage=20;aulast=Soma

Background: Although the health risks of tobacco smoking are well documented, there is increasing evidence that smokers have a low incidence of inflammatory and neurodegenerative diseases. Moreover, this reduced immunity may pave a way for increased relative risk of harboring these viral entities such as human papillomavirus (HPV) 16 and HPV 18 more specifically in oral cavity. Objective: The objective of the study was to evaluate whether tobacco smoking is associated with the prevalence of HPV 16 and HPV 18 in saliva of chronic smokers and nonsmokers. Methodology: A total of sixty participants constitute the study groups. Out of sixty participants, thirty were grouped with smoking habits, Group I (n = 30) and remaining thirty with no history of smoking, Group II (n = 30). DNA was extracted from saliva of all the participants using QIAamp “DNA mini kit.” Polymerase chain reaction was performed, using primer sequence specific for HPV 16 and HPV 18 obtained from NCBI database. The determination of HPV 16 and HPV 18 was done if and only if the bands were noticed on the ethidium bromide stained agarose gel at 120 bp for HPV 16 and 180 bp for HPV 18. Results: HPV 16 and HPV 18 were not found in both smokers and nonsmokers. Conclusion: The present study is in opinion that smoking is not associated with the HPV 16 and HPV 18 prevalence in saliva. However, the possibilities of synergistic effects of reduced immunity, as a result of smoking and increased prevalence of HPV 16 and HPV 18 in HPV-diagnosed individuals, should be addressed with a large sample.