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Updated: Jan 17, 2026

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Genes and environment profoundly affect the human virome.

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    Human genetic factors significantly influence viral load for 31 DNA viruses, particularly Epstein-Barr virus (EBV). Higher EBV load causally increases Hodgkin lymphoma risk, but not multiple sclerosis risk.

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    Area of Science:

    • Human virology
    • Genetics
    • Immunology

    Background:

    • Many viruses persist lifelong in humans, with variable viral loads impacting disease.
    • Host genetic factors play a crucial role in controlling viral abundance.

    Purpose of the Study:

    • To analyze viral load variation across 31 DNA viruses in a large human cohort.
    • To identify human genetic loci associated with viral load.
    • To investigate the causal relationship between Epstein-Barr virus (EBV) load and specific diseases.

    Main Methods:

    • Whole-genome sequencing data from UK Biobank, SPARK, and All of Us cohorts (n > 600,000).
    • Analysis of viral load for 31 DNA viruses in blood and saliva.
    • Genome-wide association studies (GWAS) to identify genetic loci linked to viral load.
    • Mendelian randomization to assess causal effects of EBV load on multiple sclerosis and Hodgkin lymphoma.

    Main Results:

    • Viral load varied significantly with age, time of day, season, and sex.
    • Dozens of human genetic loci were associated with the load of seven viruses, notably EBV (45 loci) and human herpesvirus 7 (HHV-7, 24 loci).
    • The human leukocyte antigen (HLA) complex showed the strongest associations with viral load, with specific HLA alleles demonstrating virus and site-specific effects.
    • Genes involved in antigen presentation, like ERAP1 and ERAP2, were also implicated.
    • High EBV viral load was causally linked to increased Hodgkin lymphoma risk (OR=19.81), but not multiple sclerosis risk (p=0.52).

    Conclusions:

    • Human genetic variation, particularly within the HLA complex and antigen-processing genes, profoundly impacts viral load.
    • Chronic high EBV viral load is a significant risk factor for Hodgkin lymphoma.
    • The association of EBV with autoimmune conditions likely reflects immune responses to specific viral epitopes rather than viral load itself.