| Autor: |
Manuel, Oriol, Wójtowicz, Agnieszka, Bibert, Stéphanie, Mueller, Nicolas J., van Delden, Christian, Hirsch, Hans H., Steiger, Juerg, Stern, Martin, Egli, Adrian, Garzoni, Christian, Binet, Isabelle, Weisser, Maja, Berger, Christoph, Cusini, Alexia, Meylan, Pascal, Pascual, Manuel, Bochud, Pierre-Yves, Binet, I., De Geest, S., van Delden, C., Hofbauer, GFK, Huynh-Do, U., Koller, MT, Lovis, C., Manuel, O., Meylan, P., Mueller, NJ, Pascual, M., Schaub, S., Steiger, J. |
| Jazyk: |
angličtina |
| Rok vydání: |
2017 |
| Popis: |
Background. Polymorphisms in the interferon-λ (IFNL) 3/4 region have been associated with reduced hepatitis C virus clearance. We explored the role of such polymorphisms on the incidence of CMV infection in solid-organ transplant (SOT) recipients. Methods. Caucasian patients participating in the Swiss Transplant Cohort Study in 2008-2011 were included. A novel functional TT/-G polymorphism (rs368234815) in the CpG region upstream of IFNL3 was investigated. Results. A total of 840 SOT recipients at risk for CMV were included, among whom 373 (44%) received antiviral prophylaxis. The 12-months cumulative incidence of CMV replication and disease were 0.44 and 0.08, respectively. Patient homozygous for the minor rs368234815 allele (-G/-G) tended to have a higher cumulative incidence of CMV replication (SHR=1.30 [95%CI 0.97-1.74], P=0.07) compared to other patients (TT/TT or TT/-G). The association was significant among patients followed by a preemptive approach (SHR=1.46 [1.01-2.12], P=0.047), especially in patients receiving an organ from a seropositive donor (D+, SHR=1.92 [95%CI 1.30-2.85], P=0.001), but not among those who received antiviral prophylaxis (SHR=1.13 [95%CI 0.70-1.83], P=0.6). These associations remained significant in multivariate competing risk regression models. Conclusions. Polymorphisms in the IFNL3/4 region influence susceptibility to CMV replication in SOT recipients, particularly in patients not receiving antiviral prophylaxis |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
|
