ArticleVirus evolution2018
Relational concurrency, stages of infection, and the evolution of HIV set point viral load.
Article in Virus evolution, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Evolution of HIV virulence in response to disease-modifying vaccines: A modeling study.Vaccine · 2023Article
- Why does age at HIV infection correlate with set point viral load? An evolutionary hypothesis.Epidemics · 2022Article
- Comparison of two simulators for individual based models in HIV epidemiology in a population with HSV 2 in Yaoundé (Cameroon).Scientific reports · 2021Article
- Test-and-treat coverage and HIV virulence evolution among men who have sex with men.Virus evolution · 2021Article
- Large benefits to youth-focused HIV treatment-as-prevention efforts in generalized heterosexual populations: An agent-based simulation model.PLoS computational biology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
HIV viral load (VL) predicts both transmission potential and rate of disease progression. For reasons that are still not fully understood, the set point viral load (SPVL) established after acute infection varies across individuals and populations. Previous studies have suggested that population mean SPVL (MSPVL) has evolved near an optimum that reflects a trade-off between transmissibility and host survival. Sexual network structures affect rates of potential exposure during different within-host phases of infection marked by different transmission probabilities, and thus affect the number and timing of transmission events. These structures include
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Registered trials
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