RT Journal Article
T1 HLA-B, HLA-C and KIR improve the predictive value of IFNL3 for Hepatitis C spontaneous clearance.
A1 Frias, Mario
A1 Rivero-Juarez, Antonio
A1 Rodriguez-Cano, Diego
A1 Camacho, Angela
A1 Lopez-Lopez, Pedro
A1 Risalde, Maria Angeles
A1 Manzanares-Martin, Barbara
A1 Brieva, Teresa
A1 Machuca, Isabel
A1 Rivero, Antonio
K1 Genetic markers
K1 HIV infections
K1 HLA-B44 antigen
K1 HLA-C antigens
K1 Hepacivirus
AB IFNL3 is the strongest predictor of spontaneous resolution (SR) of hepatitis C virus (HCV), however, consideration of IFNL3 genotype alone is of limited clinical value for the prediction of SR or chronic HCV infection. The objective of this study was to analyze the impact of HLA-B, HLA-C and KIRs on SR, as well as their additive effects on the predictive value of the IFNL3 genotype. We conducted a retrospective study of HIV patients that included both SR and chronic HCV patients. In our study, 61.6% of patients with IFNL3 CC achieved SR, and 81.5% with non-CC genotypes did not achieve SR. HLA-B*44, HLA-C*12, and KIR3DS1 were identified as predictive factors for SR, with percentages of 77.4%, 85.7% and 86.2%, respectively, for patients who did not experience SR. The presence of at least one of these three markers, defined as a genetically unfavorable profile (GUP), combined with the IFNL3 non-CC genotype showed a value of 100% for non-SR. The absence of the three markers, defined as a genetically favorable profile (GFP), in addition to the IFNL3 CC genotype showed a percentage of 74.1% for SR. The combination of these markers in addition to the IFNL3 genotype improves the predictive value of IFNL3 for SR of acute HCV infection in HIV patients, which would be clinically valuable.
PB Nature Publishing Group
YR 2017
FD 2017-11-27
LK http://hdl.handle.net/10668/12007
UL http://hdl.handle.net/10668/12007
LA en
NO Frias M, Rivero-Juárez A, Rodriguez-Cano D, Camacho Á, López-López P, Risalde MÁ, et al. HLA-B, HLA-C and KIR improve the predictive value of IFNL3 for Hepatitis C spontaneous clearance. Sci Rep. 2018 Jan 12;8(1):659
NO Tis work was supported by the SPANISH AIDS Research Network RD16/0025/0034-ISCIII-FEDER, Fundación Progreso y Salud de la Junta deAndalucía (0187/2013), and Fundación para la Investigación en Salud del Instituto de Salud Carlos III (PI15/01017). A.R is the recipient of a Research Support grant from the Consejería de Salud de la Junta de Andalucía (A-0025-2016).
DS RISalud
RD Apr 10, 2025