ArticlePLoS pathogens2016
The Mutational Robustness of Influenza A Virus.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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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.
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Who cites it
68 citing papers in PubMed, 114 citations in OpenAlex.
- Concepts of RNA virus evolution for the design of better antiviral countermeasures.Nature reviews. Microbiology · 2026Review
- Phylogenetic and Proteomic Analyses of Segment 2 Sequence Reveals the Presence of Two Variants of a Divergent Amnoonvirus (Family:Microorganisms · 2026Article
- Mutation rate variability in viral populations: Implications for lethal mutagenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- Stochastic intracellular replication dynamics shape population-level evolution in Influenza A Virus.Virus evolution · 2026Article
- Advanced biopolymer nanocomposites for real-time biosurveillance and defense against antimicrobial resistance and viral threats.RSC advances · 2025Review
- Viral expansion after transfer is a primary driver of influenza A virus transmission bottlenecks.PLoS biology · 2025Article
- Viral expansion after transfer is a primary driver of influenza A virus transmission bottlenecks.bioRxiv : the preprint server for biology · 2025Article
- Inhibiting kinesin family member 20A disrupts Zika virus entry by blocking internalization.Journal of microbiology (Seoul, Korea) · 2025Article
- An intranasally administered IgM protects against antigenically distinct subtypes of influenza A viruses.Nature communications · 2025Article
- Emergence, migration and spreading of the high pathogenicity avian influenza virus H5NX of the Gs/Gd lineage into America.The Journal of general virology · 2025Review
- Phylodynamics beyond neutrality: the impact of incomplete purifying selection on viral phylogenies and inference.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Article
- Human Riboviruses: A Comprehensive Study.Journal of molecular evolution · 2025Review
- Lethal mutagenesis and the transient within-host dynamics of viral adaptation.Virus evolution · 2025Article
- Influenza A virus within-host evolution and positive selection in a densely sampled household cohort over three seasons.bioRxiv : the preprint server for biology · 2024Article
- Transmission Bottleneck Size Estimation from De Novo Viral Genetic Variation.Molecular biology and evolution · 2024Article
- Influenza A virus within-host evolution and positive selection in a densely sampled household cohort over three seasons.Virus evolution · 2024Article
- Emerging roles of cytoskeletal transport and scaffold systems in human viral propagation.Animal cells and systems · 2024Review
- Deep mutational scanning reveals the functional constraints and evolutionary potential of the influenza A virus PB1 protein.Journal of virology · 2023Article
- Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
A virus' mutational robustness is described in terms of the strength and distribution of the mutational fitness effects, or MFE. The distribution of MFE is central to many questions in evolutionary theory and is a key parameter in models of molecular evolution. Here we define the mutational fitness effects in influenza A virus by generating 128 viruses, each with a single nucleotide mutation. In contrast to mutational scanning approaches, this strategy allowed us to unambiguously assign fitness values to individual mutations. The presence of each desired mutation and the absence of additional mutations were verified by next generation sequencing of each stock. A mutation was considered lethal only after we failed to rescue virus in three independent transfections. We measured the fitness of each viable mutant relative to the wild type by quantitative RT-PCR following direct competition on A549 cells. We found that 31.6% of the mutations in the genome-wide dataset were lethal and that the lethal fraction did not differ appreciably between the HA- and NA-encoding segments and the rest of the genome. Of the viable mutants, the fitness mean and standard deviation were 0.80 and 0.22 in the genome-wide dataset and best modeled as a beta distribution. The fitness impact of mutation was marginally lower in the segments coding for HA and NA (0.88 ± 0.16) than in the other 6 segments (0.78 ± 0.24), and their respective beta distributions had slightly different shape parameters. The results for influenza A virus are remarkably similar to our own analysis of CirSeq-derived fitness values from poliovirus and previously published data from other small, single stranded DNA and RNA viruses. These data suggest that genome size, and not nucleic acid type or mode of replication, is the main determinant of viral mutational fitness effects.
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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.