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Updated: Jul 3, 2025
13:56
A Comparative Approach to Characterize the Landscape of Host-Pathogen Protein-Protein Interactions
Published on: July 18, 2013
11.2K
Computational multigene interactions in virus growth and infection spread
1Wisconsin Institute for Discovery, Chemical and Biological Engineering, University of Wisconsin-Madison, 330 N. Orchard Street, Madison, WI 53715, USA.
Virus Evolution
|February 16, 2024
Summary
Virus mutations can have amplified negative effects on virus yield due to synergistic epistasis. However, these interactions show minimal impact on infection spread, highlighting how epistasis varies with fitness measures.
Area of Science:
- Virology
- Computational Biology
- Genetics
Background:
- Viruses exhibit genetic heterogeneity and large populations, aiding immune evasion and host adaptation.
- Studying viral persistence is complex due to pleiotropic mutations, unknown gene interactions, and non-standardized fitness measures.
Purpose of the Study:
- To computationally model virus cell infection and investigate the impact of gene-gene interactions among deleterious mutations on viral fitness.
- To analyze how epistasis affects different measures of viral fitness, including single-cycle growth and multicycle infection spread.
Main Methods:
- Developed a data-driven computational model of vesicular stomatitis virus (a prototype RNA virus) infection.
- Incorporated viral gene expression kinetics, gene-gene interactions, genome replication, and host resource allocation.
- Simulated deleterious mutations by perturbing biophysical parameters and analyzed effects on virus yield and infection spread.
Main Results:
- Synergistic epistasis was observed for virus yield, where deleterious mutations amplified each other's adverse effects.
- For the same mutations, multicycle infection spread exhibited weak or negligible epistasis, with mutations acting independently.
- These findings remained consistent across high- and low-host resource environments.
Conclusions:
- Different types and magnitudes of epistasis can emerge for genetically identical virus variants depending on the fitness metric used.
- Gene-gene interactions significantly influence viral growth and spread dynamics in distinct ways.
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