ArticleMicrobial risk analysis2020
A Data Simulation Method to Optimize a Mechanistic Dose-Response Model for Viral Loads of Hepatitis A.
Article in Microbial risk analysis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Research gaps and priorities for quantitative microbial risk assessment (QMRA).Risk analysis : an official publication of the Society for Risk Analysis · 2024Article
- A Somatic Coliphage Threshold Approach To Improve the Management of Activated Sludge Wastewater Treatment Plant Effluents in Resource-Limited Regions.Applied and environmental microbiology · 2020Article
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
Driven by the quantitative estimate of risk via the dose-response models, quantitative microbial risk assessment has been used successfully for public health interventions. The dose-response models are derived starting from an average exposed dose of infectious particles, this dictates the of dose data units required. Then dose-response data from animal model experiments are used to optimize these mechanistic dose-response models. For hepatitis A (Hep-A), the only available dose-response data use grams of feces for dose units. Therefore, to develop a dose-response model for Hep-A a method of converting these doses in grams of feces into infectious particles, while accounting for the uncertainty of this conversion is needed. This research develops a method to couple data simulation with the likelihood estimation method for model optimization to accomplish this. This adapted method uses data simulation to model the doses as viral particles while accounting for the within-group variability of this simulation. Then these simulated doses, coupled with the original dose-response data, are used to optimize the mechanistic dose-response models. This method results in a more computationally rigorous means of modeling these types of dose-response data. The resulting dose-response model for Hep-A is also more appropriate to use than the current option for Hep-A risk models.
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Registered trials
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