Analyses of human papillomavirus genotypes and viral loads in anogenital warts

✍ Scribed by Siolian L.R. Ball; David M. Winder; Katie Vaughan; Nashat Hanna; Jonathan Levy; Jane C. Sterling; Margaret A. Stanley; Peter K.C. Goon

• Publisher: John Wiley and Sons
• Year: 2011
• Tongue: English
• Weight: 108 KB
• Volume: 83
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/jmv.22111

✦ Synopsis

Abstract

Condylomata acuminata (genital warts) are the most common sexually transmitted viral diseases. These lesions are caused by infection with mucosal human papillomaviruses (HPVs). However, there is limited information on HPV strain distribution involved in the molecular pathogenesis of these lesions. To address this, the strain prevalence and the frequency of multiple HPV infections were determined in wart tissue obtained from 31 patients attending a wart clinic. These lesions were bisected and subjected to parallel DNA and mRNA extractions. HPV‐type prevalence and incidence of multiple infections were determined by the Roche Linear Array assay. qPCR compared HPV 6, 11, 16, and 18 viral loads and RT‐qPCR measured HPV 6 and 11 E6 genomic expression levels. Seventy‐one percent of these samples were infected with multiple HPVs. Only one sample was negative for HPV 6 or 11 DNA. Forty‐eight percent of samples were positive for a high risk (oncogenic) HPV. The results show that multiple infections in tissue are frequent and the subsequent analysis of HPV 6 and 11 E6 DNA viral loads suggested that other HPVs could be causing lesions. Further analysis of HPV 6/11 E6 mRNA levels showed that there was no discernable relationship between HPV 6 E6 DNA viral load and relative HPV 6 or 11 E6 mRNA levels thereby questioning the relevance of viral load to lesion causality. J. Med. Virol. 83:1345–1350, 2011. © 2011 Wiley‐Liss, Inc.