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Phylogenetic estimation of the viral fitness landscape of HIV-1 set-point viral load. 2022
Lele Zhao, and
Chris Wymant, and
François Blanquart, and
Tanya Golubchik, and
Astrid Gall, and
Margreet Bakker, and
Daniela Bezemer, and
Matthew Hall, and
Swee Hoe Ong, and
Jan Albert, and
Norbert Bannert, and
Jacques Fellay, and
M Kate Grabowski, and
Barbara Gunsenheimer-Bartmeyer, and
Huldrych F Günthard, and
Pia Kivelä, and
Roger D Kouyos, and
Oliver Laeyendecker, and
Laurence Meyer, and
Kholoud Porter, and
Ard van Sighem, and
Marc van der Valk, and
Ben Berkhout, and
Paul Kellam, and
Marion Cornelissen, and
Peter Reiss, and
Christophe Fraser, and
Luca Ferretti
Big Data Institute, Li Ka Shing Centre for Health Information and Discovery, Nuffield Department of Medicine, University of Oxford, Old Road Campus, Headington, Oxford OX3 7LF, UK.
Set-point viral load (SPVL), a common measure of human immunodeficiency virus (HIV)-1 virulence, is partially determined by viral genotype. Epidemiological evidence suggests that this viral property has been under stabilising selection, with a typical optimum for the virus between 104 and 105 copies of viral RNA per ml. Here we aimed to detect transmission fitness differences between viruses from individuals with different SPVLs directly from phylogenetic trees inferred from whole-genome sequences. We used the local branching index (LBI) as a proxy for transmission fitness. We found that LBI is more sensitive to differences in infectiousness than to differences in the duration of the infectious state. By analysing subtype-B samples from the Bridging the Evolution and Epidemiology of HIV in Europe project, we inferred a significant positive relationship between SPVL and LBI up to approximately 105 copies/ml, with some evidence for a peak around this value of SPVL. This is evidence of selection against low values of SPVL in HIV-1 subtype-B strains, likely related to lower infectiousness, and perhaps a peak in the transmission fitness in the expected range of SPVL. The less prominent signatures of selection against higher SPVL could be explained by an inherent limit of the method or the deployment of antiretroviral therapy.
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