Abstract

BackgroundStudies 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.MethodsWe 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.ResultsWe 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).ConclusionsFuture studies of infectious etiologies of lung cancer should look beyond HPyVs and HPVs as candidate infectious agents.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2381-3) contains supplementary material, which is available to authorized users.

Highlights

  • 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

  • The results of the regression analysis comparing the highest to the lowest quartile of Merkel cell polyomavirus (MCV) antibodies with respect to incident lung cancer found no appreciable association for either VP1 or small T antigen (ST-Ag) (Table 3)

  • Compared to men with the lowest levels of KI polyomavirus (KIV) antibodies, those with the highest quartile of VP1 and ST-Ag did not face a significantly increased risk of lung cancer. Those with the highest quartile of WU polyomavirus (WUV) VP1 and WUV ST-Ag antibodies showed no evidence of increased risk

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Summary

Introduction

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. In China, lung cancer is the most commonly diagnosed cancer in males, the second most common in females, and the leading cause of cancer related death for both sexes by a substantial margin [1]. The burden of lung cancer in China is rising, with disability-adjusted life years per 100,000 increasing by more than 50 % between 1990 (552, 95 % confidence interval (CI): 458–782) and. Air pollution (industrial emissions, cooking exhaust, second hand smoke, and residential radon), and genetics are established lung cancer risk factors that explain the majority, but not all, of this burden of disease [3, 4]. Due to the lung’s propensity for infection, it is possible that some lung cancers may have an infectious etiology.

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