It is likely that in a larger sample of LCLs, further genes would show significant correlations with relative EBV copy number. It is therefore important to control for the effects of EBV copy number in gene expression studies utilising large samples of LCLs. Other studies of the impact of EBV on the gene expression patterns of LCLs include a study by Choy et al., which reported that,15% of genes to have at least 5% of their variance correlated with EBV copy number. In a study of semi-quantitative antibody response to EBV gene EBNA1, Rubicz et al. were able to identify 15 SNPs which were associated with EBV antibody response at genome-wide significant level. In contrast, Kuparinen et al. performed a GWAS for CMV antibody response and did not identify any genome-wide significant SNPs. It is possible that a different genetic architecture underlies the host response to control of EBV copy number in LCLs than that of EBV antibody response. Additionally all of the genes associated with the EBV antibody response were within the HLA system, a region of the genome this study was not well-powered to interrogate given the differences in HLA allele frequencies between populations and our criteria that a variant must be present in all 12 populations studied for SNP inclusion. Our finding that the 1.6 M SNPs studied in this GWAS could collectively explain 65% of the variance in relative EBV copy number, while no single SNP reached genome-wide significance, suggests that many variants of small effect play a collective role within LCLs. Similarly, GWAS of genetic resistance to HIV-1 infection could not find any common variants which were protective, while GWAS of host control of HIV-1 viral load found a number of genome-wide significant loci associated with lower HIV-1 viral load set points and slower progression to AIDS. The power to identify host genetic variation of virus infection traits may greatly depend on the trait under study and the sample sizes. We estimated the heritability of relative EBV copy number, based on data from 101 parent-child trios to be 34%. Other studies have found EBV anti-EBNA1 antibody response to be 68% VE-821 heritable when considered as a discrete trait and discrete anti-VCA IgG antibody response to be 32–48% heritable. Infectious mononucleosis concordance rates in twins were estimated to be 12% between monozygotic twins and 6% between dizygotic twins. Therefore, host genetic factors appear to play a variable but significant role in symptomatic response to primary EBV infection, the adaptive immune response to EBV latency, and the cellintrinsic control of EBV latency although none of the variants previously identified were significantly associated with EBV copy number in our analysis. This study has established that relative EBV copy number within LCLs is very much a complex trait, which has a significant heritable component. Our results suggest that many genetic variants of effect size less than 4.7% of variance in relative EBV copy number exist, but which this study was not statistically powered to detect. This study also focused on 1.6 million single nucleotide polymorphisms which were common to every population studied.