ArticleChaos (Woodbury, N.Y.)2010
On the possible role of robustness in the evolution of infectious diseases.
Article in Chaos (Woodbury, N.Y.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed.
- Surface Composition and Temperature Interact to Shape Viral Survival and Growth.Environmental microbiology · 2026Article
- Phage engineering and the evolutionary arms race.Current opinion in biotechnology · 2021Review
- Discovery and characterization of variance QTLs in human induced pluripotent stem cells.PLoS genetics · 2019Article
- Adaptive Landscape by Environment Interactions Dictate Evolutionary Dynamics in Models of Drug Resistance.PLoS computational biology · 2016Article
- Evolvability and robustness in populations of RNA virus Φ6.Frontiers in microbiology · 2014Article
- ncDNA and drift drive binding site accumulation.BMC evolutionary biology · 2012Article
- Host alternation of chikungunya virus increases fitness while restricting population diversity and adaptability to novel selective pressures.Journal of virology · 2011Article
- Introduction to focus issue: genetic interactions.Chaos (Woodbury, N.Y.) · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Robustness describes the capacity for a biological system to remain canalized despite perturbation. Genetic robustness affords maintenance of phenotype despite mutational input, necessarily involving the role of epistasis. Environmental robustness is phenotypic constancy in the face of environmental variation, where epistasis may be uninvolved. Here we discuss genetic and environmental robustness, from the standpoint of infectious disease evolution, and suggest that robustness may be a unifying principle for understanding how different disease agents evolve. We focus especially on viruses with RNA genomes due to their importance in the evolution of emerging diseases and as model systems to test robustness theory. We present new data on adaptive constraints for a model RNA virus challenged to evolve in response to UV radiation. We also draw attention to other infectious disease systems where robustness theory may prove useful for bridging evolutionary biology and biomedicine, especially the evolution of antibiotic resistance in bacteria, immune evasion by influenza, and malaria parasite infections.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.