Journal of Antivirals & Antiretrovirals
Open Access
ISSN: 1948-5964
+44 1300 500008
ISSN: 1948-5964
+44 1300 500008
Rashmirani Senapati, Bhagirathi Dwibedi, Bhagyalaxmi Nayak and Shantanu Kumar Kar
ICMR, Bhubaneswar, India
Acharya Harihara Regional Cancer Centre, India
Scientific Tracks Abstracts: J Antivir Antiretrovir
HPV infection plays a central role in the development of cervical cancer. Among 184 different HPV genotypes, only 40 diverse types can infect anogenital region which can be classified into 3 classes based on their oncogenic potential. HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73 and 82 are included in high risk group while HPV6, 11, 40, 42, 43, 44, 54, 61, 70, 72 and 81 are in low risk group where as HPV 26, 53 and 66 belong to the group of intermediate risk. Cervical cancer is often associated with multiple HPV genotypes infection. Thus it is considered that co-infection may be a risk factor that drives carcinogenesis. But contradicting studies invoke confusion about the correlation between multiple infection and cervical disease. It is yet to be understood that whether the risk of cervical cancer is type specific or is it common for all the genotypes. This question is important for second generation vaccine strategy and disease management. With limited reports available, the present study aimed to investigate the risk conferred by specific hr-HPV genotypes co-infections towards invasive cervical carcinoma. 595 participants were enrolled for this study. Among them 346 were HPV positive. Among the HPV positive cases 172 were diagnosed with invasive cervical carcinoma and 174 were with normal cytology. A total of 346 samples were processed for HPV genotyping. E6/E7 multiplex nested type-specific PCR was done to detect 20 HPV genotypes. Association between the genotypes and cervical cancer was estimated by calculating the Odds ratio and 95% confidence interval. The most prevalent genotype was HPV 16 (87.28%) followed by HPV 18 (24.56%) and HPV 51 (3.46%). Other detected genotypes in descending order were HPV 39 (3.46%), HPV 66 (2.8%), HPV 68 (2.3%), HPV 35 (1.7%), HPV 45 (1.7%), HPV 44 (1.1%), HPV 58 (1.1%), HPV 52 (.57%), HPV 6/11 (.57%), HPV 42 (.57%) and HPV 43 (.57%). Prevalence of multiple genotypes was 23.41% with double, triple and quadruple genotypes while the prevalence of single genotype infection was 76.59%. Genotypes not targeted by quadrivalent vaccine types (OR=2.94 95% CI=1.48-5.80; p=.001) conferred a 2.94 fold risk of cervical carcinoma. Cases coinfected with phylogenetically related genotypes (OR=2.29; 95% CI=.69-7.59; p=.68) had 2.29 fold risk of cervical cancer. Genotypes not targeted by 9-valent vaccines (OR=.40; 95% CI=.19-.85; p=.017) conferred a lesser risk of cervical carcinoma. In conclusion, the risk of development of cervical cancer is genotype specific and might be associated with type-specific interactions between the genotypes in multiple infections.
Rashmirani Senapati is a Senior Research Fellow (Indian Council of Medical Research) and PhD student at Viral Research and Diagnostic Laboratory, Regional Medical Research Centre (ICMR), Bhubaneswar, Odisha, India. She is working on HPV genotype distribution and analysis of viral physical status in the population of Odisha, India.
Email: rasmisenapati@gmail.com