HLA-E Polymorphism Determines Susceptibility to BK Virus Nephropathy after Living-Donor Kidney Transplant

• Main Authors: Hana Rohn, Rafael Tomoya Michita, Sabine Schramm, Sebastian Dolff, Anja Gäckler, Johannes Korth, Falko M. Heinemann, Benjamin Wilde, Mirko Trilling, Peter A. Horn, Andreas Kribben, Oliver Witzke, Vera Rebmann
• Format: Article
• Language: English
• Published: MDPI AG 2019-08-01
• Series: Cells
• Subjects: BK virus; polyomavirus; nephropathy; human leukocyte antigen-E; kidney transplantation
• Online Access: https://www.mdpi.com/2073-4409/8/8/847

Human leukocyte antigen (HLA)-E is important for the regulation of anti-viral immunity. BK polyomavirus (BKPyV) reactivation after kidney transplant is a serious complication that can result in BKPyV-associated nephropathy (PyVAN) and subsequent allograft loss. To elucidate whether HLA-E polymorphisms influence BKPyV replication and nephropathy, we determined the HLA-E genotype of 278 living donor and recipient pairs. A total of 44 recipients suffered from BKPyV replication, and 11 of these developed PyVAN. Homozygosity of the recipients for the HLA-E*01:01 genotype was associated with the protection against PyVAN after transplant (<i>p</i> = 0.025, OR 0.09, CI [95%] 0.83&#8722;4.89). Considering the time course of the occurrence of nephropathy, recipients with PyVAN were more likely to carry the HLA-E*01:03 allelic variant than those without PyVAN (Kaplan&#8722;Meier analysis <i>p</i> = 0.03; OR = 4.25; CI (95%) 1.11&#8722;16.23). Our findings suggest that a predisposition based on a defined HLA-E genotype is associated with an increased susceptibility to develop PyVAN. Thus, assessing HLA-E polymorphisms may enable physicians to identify patients being at an increased risk of this viral complication.