ArticleJournal of the Royal Society, Interface2021
Life cycle process dependencies of positive-sense RNA viruses suggest strategies for inhibiting productive cellular infection.
Article in Journal of the Royal Society, Interface, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Integrative modelling of innate immune response dynamics during virus infection.PLoS computational biology · 2026Article
- A detailed kinetic model of Eastern equine encephalitis virus replication in a susceptible host cell.PLoS computational biology · 2025Article
- Rationalised experiment design for parameter estimation with sensitivity clustering.Scientific reports · 2024Article
- Deep Proteomics Network and Machine Learning Analysis of Human Cerebrospinal Fluid in Japanese Encephalitis Virus Infection.Journal of proteome research · 2023Article
- Mathematical modeling of plus-strand RNA virus replication to identify broad-spectrum antiviral treatment strategies.PLoS computational biology · 2023Article
- Interplay of Cellular mRNA, miRNA and Viral miRNA during Infection of a Cell.International journal of molecular sciences · 2022Article
- Sterile inflammation alters neutrophil kinetics in mice.Journal of leukocyte biology · 2022Article
- Mathematical modeling of plus-strand RNA virus replication to identify broad-spectrum antiviral treatment strategies.bioRxiv : the preprint server for biology · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Life cycle processes of positive-strand (+)RNA viruses are broadly conserved across families, yet they employ different strategies to grow in the cell. Using a generalized dynamical model for intracellular (+)RNA virus growth, we decipher these life cycle determinants and their dependencies for several viruses and parse the effects of viral mutations, drugs and host cell permissivity. We show that poliovirus employs rapid replication and virus assembly, whereas the Japanese encephalitis virus leverages its higher rate of translation and efficient cellular reorganization compared to the hepatitis C virus. Stochastic simulations demonstrate infection extinction if all seeding (inoculating) viral RNA degrade before establishing robust replication critical for infection. The probability of this productive cellular infection, 'cellular infectivity', is affected by virus-host processes and defined by early life cycle events and viral seeding. An increase in cytoplasmic RNA degradation and delay in vesicular compartment formation reduces infectivity, more so when combined. Synergy among these parameters in limiting (+)RNA virus infection as predicted by our model suggests new avenues for inhibiting infections by targeting the early life cycle bottlenecks.
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