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Cancer Epidemiol Biomarkers Prev. 2013 Oct;22(10):1747-55. doi: 10.1158/1055-9965.EPI-13-0240. Epub 2013 Jul 24.

Investigation of epstein-barr virus as a potential cause of B-cell non-Hodgkin lymphoma in a prospective cohort.

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  • 1Authors' Affiliations: Department of Environmental and Occupational Health, Drexel University School of Public Health, Philadelphia, Pennsylvania; Division of Public Health Sciences and Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center; Department of Epidemiology, School of Public Health and Department of Laboratory Medicine, University of Washington, Seattle, Washington; Departments of Obstetrics & Gynecology, and Microbiology, Immunology & Molecular Genetics, David Geffen School of Medicine at UCLA; Jonsson Comprehensive Cancer Center; UCLA AIDS Institute; and Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles, California.

Abstract

BACKGROUND:

We hypothesized that poor control of Epstein-Barr virus (EBV) infection, leading to reactivation of the virus, increases the risk of non-Hodgkin lymphoma (NHL) in the general population of primarily immunocompetent persons.

METHODS:

We conducted a case-control study nested within the Women's Health Initiative Observational Study cohort in which we measured antibodies to EBV antigens [immunoglobulin G (IgG) to viral capsid antigen (VCA), nuclear antigen (EBNA1), and early antigen-diffuse (EA-D)] and EBV DNA load in prediagnostic samples of 491 B-cell NHL cases and 491 controls.

RESULTS:

We found no association with established EBV infection, based on seropositivity for VCA. Seropositivity for EBNA1 was associated with decreased risk of B-cell NHL, overall [OR = 0.5; 95% confidence interval (CI), 0.3-0.8] and for each of the histologic subtypes examined. Increased risk of chronic lymphocytic leukemia (CLL) and related subtypes was observed with higher levels of EBV DNA and antibody to EA-D, both markers reflective of reactivation. These associations were strongest for cases with the shortest time interval between blood draw and diagnosis.

CONCLUSIONS:

In balance, these results do not provide strong evidence of EBV playing a causal role in B-cell NHL in general population women. The associations we observed may reflect increased risk of NHL with underlying immune impairment or could be due to reverse causation.

IMPACT:

Further characterization of the subtype-specific association with CLL is warranted. Exclusion of cases with preclinical disease markers (such as monoclonal B-lymphocytosis for CLL) may help rule out reverse causation in future studies.

PMID:
23885038
PMCID:
PMC4193346
DOI:
10.1158/1055-9965.EPI-13-0240
[PubMed - indexed for MEDLINE]
Free PMC Article
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