Latency III gene products of Epstein-Barr Virus (EBV) are associated with Systemic Lupus Erythematosus (SLE) genetic risk loci

SLE affects millions with increasing diagnostic prevalence. Genetic studies have identified >600 mostly regulatory variant associations. EBV has been nominated as a causal factor for SLE from immunochemistry and epidemiologic studies. EBNA2 concentrates at SLE risk loci (Nat Genet 50:699 2018) su...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2020-05, Vol.204 (1_Supplement), p.141-141.2
Main Authors: Laurynenka, Viktoryia, Chen, Xiaoting, Carter, Martha, Parameswaran, Sreeja, Eswar, Shruti, Kaufman, Kenneth M., Namjou, Bahram, Weirauch, Matthew T., Kottyan, Leah C., Harley, John B.
Format: Article
Language:English
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Summary:SLE affects millions with increasing diagnostic prevalence. Genetic studies have identified >600 mostly regulatory variant associations. EBV has been nominated as a causal factor for SLE from immunochemistry and epidemiologic studies. EBNA2 concentrates at SLE risk loci (Nat Genet 50:699 2018) suggesting mechanisms. Additional evidence supporting EBV as an SLE origin would advance this hypothesis of etiology. Previous simulation using our RELI algorithm revealed an astonishing association with Epstein-Barr virus nuclear antigen 2 (EBNA2) (OR=5.96, Pc=E-25) (Nat Genet 50:699, 2018). The >100 risk alleles associated at p
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.204.Supp.141.2