ArticlePLoS pathogens2022
Beneficial effects of cellular coinfection resolve inefficiency in influenza A virus transcription.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Virion aggregation shapes infection dynamics and evolutionary potential.Journal of virology · 2025Article
- Bat things come in threes: within-host dynamics of herpesvirus triple infection in bats.Journal of virology · 2025Article
- 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
- Virion aggregation shapes infection dynamics and evolutionary potential.bioRxiv : the preprint server for biology · 2025Article
- Incorporating Intracellular Processes in Virus Dynamics Models.Microorganisms · 2024Review
- Influenza A virus coinfection dynamics are shaped by distinct virus-virus interactions within and between cells.PLoS pathogens · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
For diverse viruses, cellular infection with single vs. multiple virions can yield distinct biological outcomes. We previously found that influenza A/guinea fowl/Hong Kong/WF10/99 (H9N2) virus (GFHK99) displays a particularly high reliance on multiple infection in mammalian cells. Here, we sought to uncover the viral processes underlying this phenotype. We found that the need for multiple infection maps to amino acid 26K of the viral PA protein. PA 26K suppresses endonuclease activity and viral transcription, specifically within cells infected at low multiplicity. In the context of the higher functioning PA 26E, inhibition of PA using baloxavir acid augments reliance on multiple infection. Together, these data suggest a model in which sub-optimal activity of the GFHK99 endonuclease results in inefficient priming of viral transcription, an insufficiency which can be overcome with the introduction of additional viral ribonucleoprotein templates to the cell. More broadly, the finding that deficiency in a core viral function is ameliorated through multiple infection suggests that the fitness effects of many viral mutations are likely to be modulated by multiplicity of infection, such that the shape of fitness landscapes varies with viral densities.
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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.