Phylogenetic estimation of the viral fitness landscape of HIV-1 set-point viral load.
Détails
Télécharger: 35402002_BIB_DED149CC980B.pdf (910.09 [Ko])
Etat: Public
Version: Final published version
Licence: CC BY 4.0
Etat: Public
Version: Final published version
Licence: CC BY 4.0
ID Serval
serval:BIB_DED149CC980B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Phylogenetic estimation of the viral fitness landscape of HIV-1 set-point viral load.
Périodique
Virus evolution
ISSN
2057-1577 (Print)
ISSN-L
2057-1577
Statut éditorial
Publié
Date de publication
2022
Peer-reviewed
Oui
Volume
8
Numéro
1
Pages
veac022
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: epublish
Publication Status: epublish
Résumé
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 10 <sup>4</sup> and 10 <sup>5</sup> 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 10 <sup>5</sup> 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.
Mots-clé
HIV-1, between-host evolution, set-point viral load, tansmission fitness
Pubmed
Web of science
Open Access
Oui
Création de la notice
29/04/2022 17:55
Dernière modification de la notice
08/08/2024 6:41