Rémy Rodriguez, B. Fournier, D. J. Cordeiro, Sarah Winter, K. Izawa, Emmanuel Martin, D. Boutboul, C. Lenoir, S. Fraitag, S. Kracker, T. Watts, C. Picard, J. Bruneau, I. Callebaut, A. Fischer, B. Neven, S. Latour
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Concomitant PIK3CD and TNFRSF9 deficiencies cause chronic active Epstein-Barr virus infection of T cells
Identification of biallelic loss-of-function mutations in TNFRSF9 and PIK3CD in a kindred with chronic active Epstein-Barr virus infection of T cells (CAEBV) suggests that CAEBV is the consequence of factors providing growth advantage to EBV-infected T cells combined with defective cell immunity toward EBV-infected cells.
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