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Viral genetic variation accounts for a third of variability in HIV-1 set-point viral load in Europe

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Blanquart, François | Wymant, Chris | Cornelissen, Marion | Gall, Astrid | Bakker, Margreet | Bezemer, Daniela | Hall, Matthew | Hillebregt, Mariska | Ong, Swee, Hoe | Albert, Jan | Bannert, Norbert | Fellay, Jacques | Fransen, Katrien | Gourlay, Annabelle, J | Grabowski, M. Kate | Gunsenheimer-Bartmeyer, Barbara | Günthard, Huldrych, F | Kivelä, Pia | Kouyos, Roger | Laeyendecker, Oliver | Liitsola, Kirsi | Meyer, Laurence | Porter, Kholoud | Ristola, Matti | van Sighem, Ard | Vanham, Guido | Berkhout, Ben | Kellam, Paul | Reiss, Peter | Fraser, Christophe

Edité par CCSD ; Public Library of Science -

International audience. HIV-1 set-point viral load-the approximately stable value of viraemia in the first years of chronic infection-is a strong predictor of clinical outcome and is highly variable across infected individuals. To better understand HIV-1 pathogenesis and the evolution of the viral population, we must quantify the heritability of set-point viral load, which is the fraction of variation in this phenotype attributable to viral genetic variation. However, current estimates of heritability vary widely, from 6% to 59%. Here we used a dataset of 2,028 seroconverters

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