ArticleInfectious Disease Modelling2018
A signature for biological heterogeneity in susceptibility to HIV infection?
Article in Infectious Disease Modelling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Relative infectiousness of SARS-CoV-2 vaccine breakthrough infections, reinfections, and primary infections.Nature communications · 2022Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Data on female sex workers and sero-discordant couples indicate a pattern of waning of the risk of HIV infection with longer duration of exposure to infected partners. Understanding risk of HIV acquisition and transmission is critical to understanding HIV epidemiology and informing prevention interventions. Informed by empirical data, we aimed to develop a statistical model to explain these observations. In our proposed model, the time to infection for each individual is exponentially distributed, but the marginal (population averaged) distribution of time to infection follows a Weibull distribution with shape parameter of about 0.5, and with the Lévy distribution being the mixing distribution. Simulations based on this model demonstrated how HIV epidemics are destined to emerge rapidly, because of the rapid sero-conversion upon exposure, but also simultaneously destined to saturate and decline rapidly after emergence, just as observed for the HIV epidemics in sub-Saharan Africa. These results imply considerable individual variability in infection risk, probably because of biological heterogeneity in the susceptibility to HIV infection. Factoring this variability in mathematical models, through the methodology provided here, could be critical for valid estimations of impact of HIV interventions and assessments of cost-effectiveness.
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