Absence of an association of human polyomavirus and papillomavirus infection with lung cancer in China: a nested case–control study. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Colombara, Danny; Manhart, Lisa; Carter, Joseph; Hawes, Stephen; Weiss, Noel; Hughes, James; Qiao, You-Lin; Taylor, Philip; Smith, Jennifer; Galloway, Denise
• Is Part Of: BMC cancer. Volume 16:Issue 1(2016)
• Page Start: 1
• Page End: 11
• Publication Date: 2016-12
• Subjects: Lung cancer -- Human polyomavirus -- KI polyomavirus -- WU polyomavirus -- Merkel cell polyomavirus -- Human papillomavirus; Cancer -- Periodicals; 616.994005
• DOI: 10.1186/s12885-016-2381-3
• Languages: English
• ISSNs: 1471-2407

Abstract

Abstract Background Studies of human polyomavirus (HPyV) infection and lung cancer are limited and those regarding the association of human papillomavirus (HPV) infection and lung cancer have produced inconsistent results. Methods We conducted a nested case–control study to assess the association between incident lung cancer of various histologies and evidence of prior infection with HPyVs and HPVs. We selected serum from 183 cases and 217 frequency matched controls from the Yunnan Tin Miner's Cohort study, which was designed to identify biomarkers for early detection of lung cancer. Using multiplex liquid bead microarray (LBMA) antibody assays, we tested for antibodies to the VP1 structural protein and small T antigen (ST-Ag) of Merkel cell, KI, and WU HPyVs. We also tested for antibodies against HPV L1 structural proteins (high-risk types 16, 18, 31, 33, 52, and 58 and low-risk types 6 and 11) and E6 and E7 oncoproteins (high risk types 16 and 18). Measures of antibody reactivity were log transformed and analyzed using logistic regression. Results We found no association between KIV, WUV, and MCV antibody levels and incident lung cancer (P-corrected for multiple comparisons >0.10 for all trend tests). We also found no association with HPV-16, 18, 31, 33, 52, and 58 seropositivity (P-corrected for multiple comparisons >0.05 for all). Conclusions Future studies of infectious etiologies of lung cancer should look beyond HPyVs and HPVs as candidate infectious agents.