ArticleMolecular biology and evolution2018
Dissecting HIV Virulence: Heritability of Setpoint Viral Load, CD4+ T-Cell Decline, and Per-Parasite Pathogenicity.
Article in Molecular biology and evolution, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Clinical trial simulation of antiviral drugs.Journal of virology · 2026Review
- Phylogenetics and molecular evolution to understand and curb the HIV pandemic.Nature reviews. Microbiology · 2026Review
- Attenuation of HIV severity by slightly deleterious mutations can explain the long-term trajectory of virulence evolution.PLoS computational biology · 2025Article
- The genetic architecture of HIV-1 virulence.Virus evolution · 2025Article
- Evidence for circulation of high-virulence HIV-1 subtype B variants in the United Kingdom.Virus evolution · 2025Article
- Reconciling founder variant multiplicity of HIV-1 infection with the rate of CD4Journal of the Royal Society, Interface · 2024Article
- Virulence decomposition for bifurcating infections.Proceedings. Biological sciences · 2023Article
- Per-pathogen virulence of HIV-1 subtypes A, C and D.Proceedings. Biological sciences · 2023Article
- Mechanisms of damage prevention, signalling and repair impact disease tolerance.Proceedings. Biological sciences · 2022Article
- Decomposing virulence to understand bacterial clearance in persistent infections.Nature communications · 2022Article
- A Phylogeny-aware GWAS Framework to Correct for Heritable Pathogen Effects on Infectious Disease Traits.Molecular biology and evolution · 2022Article
- Transmitted HIV-1 is more virulent in heterosexual individuals than men-who-have-sex-with-men.PLoS pathogens · 2022Article
- Phylogenetic estimation of the viral fitness landscape of HIV-1 set-point viral load.Virus evolution · 2022Article
- Inferring Phenotypic Trait Evolution on Large Trees With Many Incomplete Measurements.Journal of the American Statistical Association · 2022Article
- Human Immunotypes Impose Selection on Viral Genotypes Through Viral Epitope Specificity.The Journal of infectious diseases · 2021Article
- Virologic Outcomes Among People Living With Human Immunodeficiency Virus With High Pretherapy Viral Load Burden Initiating on Common Core Agents.Open forum infectious diseases · 2021Article
- Heritability of the HIV-1 reservoir size and decay under long-term suppressive ART.Nature communications · 2020Article
- Increasing prevalence and local transmission of non-B HIV-1 subtypes in the French Antilles and French Guiana between 1995 and 2018.Virus evolution · 2020Article
- Proliferation and benevolence-A framework for dissecting the mechanisms of microbial virulence and health promotion.Evolutionary applications · 2020Article
- TheFuture virology · 2020Review
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22 authors.
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No grant is acknowledged in the PubMed record.
Abstract
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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