ArticlemBio2018
Influenza A Virus Superinfection Potential Is Regulated by Viral Genomic Heterogeneity.
Article in mBio, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Neuraminidase of influenza A viruses induces global desialylation of host cells via its intracellular function.Microbiology spectrum · 2026Article
- Borna disease virus 2 maintains genomic polymorphisms by superinfection in persistently infected cells.Npj viruses · 2025Article
- SARS-CoV-2 cellular coinfection is limited by superinfection exclusion.Journal of virology · 2025Article
- Exploring viral respiratory coinfections: Shedding light on pathogen interactions.PLoS pathogens · 2024Article
- When influenza viruses don't play well with others.Nature · 2023Article
- Influenza A virus coinfection dynamics are shaped by distinct virus-virus interactions within and between cells.PLoS pathogens · 2023Article
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- Article
- Semi-infectious particles contribute substantially to influenza virus within-host dynamics when infection is dominated by spatial structure.Virus evolution · 2023Article
- Heterogeneity in viral populations increases the rate of deleterious mutation accumulation.Genetics · 2022Article
- Interactions between Influenza A Virus Nucleoprotein and Gene Segment Untranslated Regions Facilitate Selective Modulation of Viral Gene Expression.Journal of virology · 2022Article
- Library-based analysis reveals segment and length dependent characteristics of defective influenza genomes.PLoS pathogens · 2021Article
- Influenza B Virus Infection Is Enhanced Upon Heterotypic Co-infection With Influenza A Virus.Frontiers in microbiology · 2021Article
- Cellular co-infection can modulate the efficiency of influenza A virus production and shape the interferon response.PLoS pathogens · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Defining the specific factors that govern the evolution and transmission of influenza A virus (IAV) populations is of critical importance for designing more-effective prediction and control strategies. Superinfection, the sequential infection of a single cell by two or more virions, plays an important role in determining the replicative and evolutionary potential of IAV populations. The prevalence of superinfection during natural infection and the specific mechanisms that regulate it remain poorly understood. Here, we used a novel single virion infection approach to directly assess the effects of individual IAV genes on superinfection efficiency. Rather than implicating a specific viral gene, this approach revealed that superinfection susceptibility is determined by the total number of viral gene segments expressed within a cell. IAV particles that express a complete set of viral genes potently inhibit superinfection, while semi-infectious particles (SIPs) that express incomplete subsets of viral genes do not. As a result, virus populations that contain more SIPs undergo more-frequent superinfection. We further demonstrate that viral replicase activity is responsible for inhibiting subsequent infection. These findings identify both a major determinant of IAV superinfection potential and a prominent role for SIPs in promoting viral coinfection.
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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.