A new paper was published in Nature on the 28 January 2026, titled, ‘Population-scale sequencing resolves determinants of persistent EBV DNA.' See comments from Dr Charles Shepherd, MEA Hon. Medical Adviser, below.
Extracts from MSK Press Release
Epstein-Barr virus (EBV) infects nearly everyone, and for most people it hides quietly in the body for life. But for some, this common virus can do far more than linger and is linked to increased risk of developing chronic diseases of the lung and heart, lupus, and certain cancers.
A new collaborative research study by researchers at Memorial Sloan Kettering Cancer Center (MSK), AstraZeneca, and Baylor College of Medicine, has identified 22 specific genetic variants that are linked to both higher active levels of EBV and chronic disease risk. The team discovered that the genetic differences — many in immune-system genes — could make it harder for the body to keep EBV under control. People with these genetic variants might be more likely to develop chronic EBV-related ailments.
Traces of viral DNA are generally dismissed as “noise” and cast aside when researchers run a typical whole-genome analysis. But rather than ignoring the EBV DNA, Dr. Lareau and his colleagues used a novel computational method to quantify how much of this genetic material was circulating in the blood. They found that EBV DNA levels vary among individuals and are influenced by genetic factors, particularly those related to the immune system.
Abstract
Epstein–Barr virus (EBV) is an endemic herpesvirus implicated in autoimmunity, cancer and neurological disorders. Although primary infection is often subclinical, persistent EBV infection can drive immune dysregulation and long-term complications.
Despite the ubiquity of infection, the determinants of EBV persistence following primary exposure remain poorly understood, although human genetic variation partially contributes to this phenotypic spectrum. Here we demonstrate that existing whole genome sequencing (WGS) data of human populations can be used to quantify persistent EBV DNA. Using WGS and health record data from the UK Biobank (n = 490,560) and All of Us (n = 245,394), we uncover reproducible associations between blood-derived EBV DNA quantifications and respiratory, autoimmune, neurological and cardiovascular diseases.
We evaluate genetic determinants of persistent EBV DNA via genome association studies, revealing heritability enrichment in immune-associated regulatory regions and protein-altering variants in 148 genes. Single-cell and pathway level analyses of these loci implicate variable antigen processing as a primary determinant of EBV DNA persistence.
Further, relevant gene programs were enriched in B cells and antigen-presenting cells, consistent with their roles in viral reservoir and clearance. Human leukocyte antigen genotyping and predicted viral epitope presentation affinities implicate major histocompatibility complex class II variation as a key modulator of EBV persistence.
Together, our analyses demonstrate how re-analysis of human population-scale WGS data can elucidate the genetic architecture of viral DNA persistence, a framework generalizable to the broader human virome.
MEA Comment:
Epstein Barr virus (EBV) is a very common herpes virus that is well known for causing glandular fever, – the ‘kissing disease' in children and young people. It is also a well recognised trigger factor for causing ME/CFS – especially in young people
EBV is an interesting virus in that it can remain in the body and there is now very strong evidence that it is linked to the development of some types of cancer such as Burkitt's lymphoma. There is also growing evidence of a link to autoimmune conditions such as lupus and rheumatoid arthritis and multiple sclerosis.
This new research, which has been published in Nature, has identified 22 genes that appear to increase the risk of developing several conditions in later life in people who have caught EBV in the past. The research also points to a link with fatigue. So it possible that these genes play a role in increasing the risk of someone developing ME/CFS after catching glandular fever.
The research adds further weight to the need to develop a vaccine against EBV and effective forms of antiviral treatment against this very common infection.
Dr Charles Shepherd,
Trustee and Hon. Medical Adviser to the ME Association,
Member of the 2018-2021 NICE guideline on ME/CFS committee,
Member of the 2002 Chief Medical Officer's Working Group on ME/CFS
Further Coverage:
- Medical Xpress: DNA research uncovers 22 genes that could put people at risk of long-term health conditions | January 28, 2026
- Science Media Centre: Expert reaction to study using population whole genome sequencing data to find genetic determinants of persistent EBV DNA and associations with chronic conditions | January 28, 2026
- NewScientist: This virus infects most of us – but why do only some get very ill? | January 28, 2026
- Financial Times(Paywalled): Scientists link 22 genes to deadly risks from common virus | January 28, 2026
- Bloomberg (Paywalled): Scientists Inch Closer To Solving The Kissing Disease Mystery | January 28, 2026