Role of genetic susceptibility to latent adenoviral infection and decreased lung function

Summary Background Latent adenoviral infection may amplify cigarette smoke-induced lung inflammation and therefore play an important role in the development of chronic obstructive pulmonary disease (COPD). Adenoviruses can evade the human immune response via their 19-kDa protein (19K) which delays the expression of class I human leukocyte antigen ( HLA ) proteins. The 19K protein shows higher affinity to HLA-B7 and A2 compared with HLA-A1 and A3 . The receptor for adenovirus ( CXADR ) and integrin β 5 ( ITGB5 ) are host factors which might affect adenovirus infection. Therefore, we investigated the contribution of HLA , CXADR , and ITGB5 genetic variants to the presence of the E1A gene and to level of lung function. Methods Study subjects were assayed for HLA-B7 , A1 , A2 and A3 by PCR-based assays using allele-specific primers. Polymorphisms of the CXADR and ITGB5 genes were genotyped by PCR-based restriction fragment length polymorphism assays. Detection of adenoviral E1A gene was performed by a real-time PCR TaqMan assay. Results E1A positive individuals had a lower FEV 1 compared with E1A negative individuals. However, there was no significant difference in E1A positivity rate between the high ( HLA-B7 and A2 ) and low ( HLA-A1 and A3 ) 19K affinity groups. There was also no significant difference in FEV 1 level between each affinity group. There was no significant difference in E1A positivity rate or lung function among the CXADR and ITGB5 genotypes. Conclusions Genetic variants in HLA , CXADR and ITGB5 do not influence latent adenoviral infections and are not associated with COPD.