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Statistical Mechanics and Thermodynamics of Viral Evolution.

Jones BA, Lessler J, Bianco S, Kaufman JH - PLoS ONE (2015)

Bottom Line: The paper analyzes a model of viral infection and evolution using the "grand canonical ensemble" and formalisms from statistical mechanics and thermodynamics.This paper also reveals a universal relationship that relates the order parameter (as a measure of mutational robustness) to evolvability in agreement with recent experimental and theoretical work.Given that real viruses have finite length RNA segments that encode proteins which determine virus fitness, the approach used here could be refined to apply to real biological systems, perhaps providing insight into immune escape, the emergence of novel pathogens and other results of viral evolution.

View Article: PubMed Central - PubMed

Affiliation: Almaden Research Center, IBM, San Jose, California, United States of America.

ABSTRACT
This paper uses methods drawn from physics to study the life cycle of viruses. The paper analyzes a model of viral infection and evolution using the "grand canonical ensemble" and formalisms from statistical mechanics and thermodynamics. Using this approach we enumerate all possible genetic states of a model virus and host as a function of two independent pressures-immune response and system temperature. We prove the system has a real thermodynamic temperature, and discover a new phase transition between a positive temperature regime of normal replication and a negative temperature "disordered" phase of the virus. We distinguish this from previous observations of a phase transition that arises as a function of mutation rate. From an evolutionary biology point of view, at steady state the viruses naturally evolve to distinct quasispecies. This paper also reveals a universal relationship that relates the order parameter (as a measure of mutational robustness) to evolvability in agreement with recent experimental and theoretical work. Given that real viruses have finite length RNA segments that encode proteins which determine virus fitness, the approach used here could be refined to apply to real biological systems, perhaps providing insight into immune escape, the emergence of novel pathogens and other results of viral evolution.

No MeSH data available.


Related in: MedlinePlus

Virus Life Cycle.The changing states of all viruses must be computed self-consistently over the entire virus life cycle. The figure shows three important stages of the model virus life cycle: (I) Infection (entering the cell), (Ξ) Immune Clearance, and (R) Reproduction and exiting the cell. Also shown are the equations for cell occupancy at each stage.
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pone.0137482.g002: Virus Life Cycle.The changing states of all viruses must be computed self-consistently over the entire virus life cycle. The figure shows three important stages of the model virus life cycle: (I) Infection (entering the cell), (Ξ) Immune Clearance, and (R) Reproduction and exiting the cell. Also shown are the equations for cell occupancy at each stage.

Mentions: In our simplified model of viral infection and replication the system of viruses passes through three stages in discrete generations (Fig 2). Free viruses first infect cells, passing into the post-infection stage, I. Some proportion of infected cells are then “killed” by the immune system, and instantly replaced by uninfected cells, and we enter the post-immunity stage, Ξ. Finally, viruses replicate and exit the cell, and we enter the post-reproduction/pre-infection stage, R. The system state in each stage can be described completely by two interacting sets of variables: the occupation of the host cells, and the distribution of “free” viruses in the environment. The self-consistent (steady state) solution for the virus life cycle is one in which each state remains unchanged after completing a full cycle.


Statistical Mechanics and Thermodynamics of Viral Evolution.

Jones BA, Lessler J, Bianco S, Kaufman JH - PLoS ONE (2015)

Virus Life Cycle.The changing states of all viruses must be computed self-consistently over the entire virus life cycle. The figure shows three important stages of the model virus life cycle: (I) Infection (entering the cell), (Ξ) Immune Clearance, and (R) Reproduction and exiting the cell. Also shown are the equations for cell occupancy at each stage.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4589373&req=5

pone.0137482.g002: Virus Life Cycle.The changing states of all viruses must be computed self-consistently over the entire virus life cycle. The figure shows three important stages of the model virus life cycle: (I) Infection (entering the cell), (Ξ) Immune Clearance, and (R) Reproduction and exiting the cell. Also shown are the equations for cell occupancy at each stage.
Mentions: In our simplified model of viral infection and replication the system of viruses passes through three stages in discrete generations (Fig 2). Free viruses first infect cells, passing into the post-infection stage, I. Some proportion of infected cells are then “killed” by the immune system, and instantly replaced by uninfected cells, and we enter the post-immunity stage, Ξ. Finally, viruses replicate and exit the cell, and we enter the post-reproduction/pre-infection stage, R. The system state in each stage can be described completely by two interacting sets of variables: the occupation of the host cells, and the distribution of “free” viruses in the environment. The self-consistent (steady state) solution for the virus life cycle is one in which each state remains unchanged after completing a full cycle.

Bottom Line: The paper analyzes a model of viral infection and evolution using the "grand canonical ensemble" and formalisms from statistical mechanics and thermodynamics.This paper also reveals a universal relationship that relates the order parameter (as a measure of mutational robustness) to evolvability in agreement with recent experimental and theoretical work.Given that real viruses have finite length RNA segments that encode proteins which determine virus fitness, the approach used here could be refined to apply to real biological systems, perhaps providing insight into immune escape, the emergence of novel pathogens and other results of viral evolution.

View Article: PubMed Central - PubMed

Affiliation: Almaden Research Center, IBM, San Jose, California, United States of America.

ABSTRACT
This paper uses methods drawn from physics to study the life cycle of viruses. The paper analyzes a model of viral infection and evolution using the "grand canonical ensemble" and formalisms from statistical mechanics and thermodynamics. Using this approach we enumerate all possible genetic states of a model virus and host as a function of two independent pressures-immune response and system temperature. We prove the system has a real thermodynamic temperature, and discover a new phase transition between a positive temperature regime of normal replication and a negative temperature "disordered" phase of the virus. We distinguish this from previous observations of a phase transition that arises as a function of mutation rate. From an evolutionary biology point of view, at steady state the viruses naturally evolve to distinct quasispecies. This paper also reveals a universal relationship that relates the order parameter (as a measure of mutational robustness) to evolvability in agreement with recent experimental and theoretical work. Given that real viruses have finite length RNA segments that encode proteins which determine virus fitness, the approach used here could be refined to apply to real biological systems, perhaps providing insight into immune escape, the emergence of novel pathogens and other results of viral evolution.

No MeSH data available.


Related in: MedlinePlus