Dissecting HIV Virulence: Heritability of Setpoint Viral Load, CD4+ T-Cell Decline, and Per-Parasite Pathogenicity
Frederic Bertels, Alex Marzel, Gabriel Leventhal, Venelin Mitov, Jacques Fellay, Huldrych F Günthard, Jürg Böni, Sabine Yerly, Thomas Klimkait, Vincent Aubert, Manuel Battegay, Andri Rauch, Matthias Cavassini, Alexandra Calmy, Enos Bernasconi, Patrick Schmid, Alexandra U Scherrer, Viktor Müller, Sebastian Bonhoeffer, Roger Kouyos, Roland R Regoes & Swiss HIV Cohort Study
abstract
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Pathogen strains may differ in virulence because they attain
different loads in their hosts, or because they induce different
disease-causing mechanisms independent of their load. In
evolutionary ecology, the latter is referred to as
"per-parasite pathogenicity". Using viral load and CD4+
T-cell measures from 2014 HIV-1 subtype B-infected individuals
enrolled in the Swiss HIV Cohort Study, we investigated if
virulence-measured as the rate of decline of CD4+ T cells-and
per-parasite pathogenicity are heritable from donor to recipient. We
estimated heritability by donor-recipient regressions applied to 196
previously identified transmission pairs, and by phylogenetic mixed
models applied to a phylogenetic tree inferred from HIV pol
sequences. Regressing the CD4+ T-cell declines and per-parasite
pathogenicities of the transmission pairs did not yield heritability
estimates significantly different from zero. With the phylogenetic
mixed model, however, our best estimate for the heritability of the
CD4+ T-cell decline is 17% (5-30%), and that of the per-parasite
pathogenicity is 17% (4-29%). Further, we confirm that the set-point
viral load is heritable, and estimate a heritability of 29%
(12-46%). Interestingly, the pattern of evolution of all these
traits differs significantly from neutrality, and is most consistent
with stabilizing selection for the set-point viral load, and with
directional selection for the CD4+ T-cell decline and the
per-parasite pathogenicity. Our analysis shows that the viral
genotype affects virulence mainly by modulating the per-parasite
pathogenicity, while the indirect effect via the set-point viral
load is minor.
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citation
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Bertels F, Marzel A, Leventhal G, Mitov V, Fellay J, Günthard H F,
Böni J, Yerly S, Klimkait T, Aubert V, Battegay M, Rauch A,
Cavassini M, Calmy A, Bernasconi E, Schmid P, Scherrer A U, Müller
V, Bonhoeffer S, Kouyos R, Regoes R R, Swiss HIV Cohort Study .
Dissecting HIV Virulence: Heritability of Setpoint Viral Load, CD4+
T-Cell Decline, and Per-Parasite Pathogenicity. Mol Biol Evol 2018;
35:27-37.
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type
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journal paper/review (English)
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date of publishing
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01-1-2018
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journal title
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Mol Biol Evol (35/1)
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ISSN electronic
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1537-1719
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pages
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27-37
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PubMed
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29029206
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DOI
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10.1093/molbev/msx246
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