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Modeling viral coevolution: HIV multi-clonal persistence and competition dynamics
Populations and Evolution · Submitted 7 Sep 2005
abstract compiled · 2026-09-23 · no language-model review
The authors' main claim The immune response induces a competition among similar phenotypes, leading to differentiation (quasi-speciation), escape dynamics and complex oscillations of viral strain abundance.
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The abstract, sentence by sentence
The coexistence of different viral strains (quasispecies) within the same host are nowadays observed for a growing number of viruses, most notably HIV, Marburg and Ebola, but the conditions for the formation and survival of new strains have not yet been understood. We present a model of HIV quasispecies competition, that describes the conditions of viral quasispecies coexistence under different immune system conditions. Our model incorporates both T and B cells responses, and we show that the role of B cells is important and additive to that of T cells. Simulations of coinfection (simultaneous infection) and superinfection (delayed secondary infection) scenarios in the early stages (days) and in the late stages of the infection (years) are in agreement with emerging molecular biology findings. The immune response induces a competition among similar phenotypes, leading to differentiation (quasi-speciation), escape dynamics and complex oscillations of viral strain abundance. We found that the quasispecies dynamics after superinfection or coinfection has time scales of several months and becomes even slower when the immune system response is weak. Our model represents a general framework to study the speed and distribution of HIV quasispecies during disease progression, vaccination and therapy.
background contribution method result interpretation main claim
| # | sentence | role | the authors' own work | states the main conclusion | strength |
|---|---|---|---|---|---|
| s0 | The coexistence of different viral strains (quasispecies) within the same host are nowadays observed for a growing number of viruses, most notably HIV, Marburg and Ebola, but the conditions for the formation and survival of new strains have not yet been understood. | background 0.51 | 0.04 | 0.03 | asserted 1.00 |
| s1 | We present a model of HIV quasispecies competition, that describes the conditions of viral quasispecies coexistence under different immune system conditions. | contribution 0.84 | 0.94 | 0.10 | asserted 0.95 |
| s2 | Our model incorporates both T and B cells responses, and we show that the role of B cells is important and additive to that of T cells. | result 0.57 | 0.93 | 0.20 | asserted 1.00 |
| s3 | Simulations of coinfection (simultaneous infection) and superinfection (delayed secondary infection) scenarios in the early stages (days) and in the late stages of the infection (years) are in agreement with emerging molecular biology findings. | result 0.89 | 0.89 | 0.09 | asserted 0.87 |
| s4 | The immune response induces a competition among similar phenotypes, leading to differentiation (quasi-speciation), escape dynamics and complex oscillations of viral strain abundance. | result 0.77 | 0.74 | 0.36 | asserted 1.00 |
| s5 | We found that the quasispecies dynamics after superinfection or coinfection has time scales of several months and becomes even slower when the immune system response is weak. | result 1.00 | 0.96 | 0.19 | asserted 1.00 |
| s6 | Our model represents a general framework to study the speed and distribution of HIV quasispecies during disease progression, vaccination and therapy. | contribution 0.40 | 0.62 | 0.16 | asserted 1.00 |
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Original abstract
The coexistence of different viral strains (quasispecies) within the same host are nowadays observed for a growing number of viruses, most notably HIV, Marburg and Ebola, but the conditions for the formation and survival of new strains have not yet been understood. We present a model of HIV quasispecies competition, that describes the conditions of viral quasispecies coexistence under different immune system conditions. Our model incorporates both T and B cells responses, and we show that the role of B cells is important and additive to that of T cells. Simulations of coinfection (simultaneous infection) and superinfection (delayed secondary infection) scenarios in the early stages (days) and in the late stages of the infection (years) are in agreement with emerging molecular biology findings. The immune response induces a competition among similar phenotypes, leading to differentiation (quasi-speciation), escape dynamics and complex oscillations of viral strain abundance. We found that the quasispecies dynamics after superinfection or coinfection has time scales of several months and becomes even slower when the immune system response is weak. Our model represents a general framework to study the speed and distribution of HIV quasispecies during disease progression, vaccination and therapy.
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