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Complementation and epistasis in viral coinfection dynamics.

Hong Gao¹, Marcus W Feldman

¹Department of Genetics, Stanford University School of Medicine, Stanford, California 94305, USA.

|March 10, 2009

Summary

Coinfection in RNA viruses, through complementation, can hinder the removal of harmful mutations. However, this phenomenon also boosts viral diversity and robustness, especially when interacting with mutation, selection, and epistasis.

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Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus

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Published on: October 7, 2011

Area of Science:

Virology
Evolutionary Biology
Genetics

Background:

Coinfection is common in RNA virus populations, leading to complementation and recombination.
Complementation significantly impacts the selection against deleterious mutations, potentially delaying their removal.
This delay suggests coinfection might negatively affect viral population evolution.

Purpose of the Study:

To investigate the interplay between complementation and other evolutionary factors (mutation, selection, epistasis) in RNA virus populations.
To understand the mechanisms driving these interactions.
To assess the net effect of complementation on viral population fitness, diversity, and robustness.

Main Methods:

Deterministic modeling of viral population dynamics.
Stochastic simulations to account for random effects.
Analysis of interactions between complementation, mutation, selection, and epistasis.

Main Results:

Strong complementation slightly reduces the overall fitness of RNA virus populations.
Complementation substantially enhances viral population diversity.
Complementation significantly improves viral population robustness, particularly when combined with selection and epistasis.

Conclusions:

While complementation may slightly decrease viral fitness, its positive effects on diversity and robustness are significant.
The interaction between complementation and evolutionary factors like selection and epistasis is crucial for understanding viral evolution.
Coinfection, via complementation, plays a complex role in shaping RNA virus population dynamics.