dorsal/arxiv
View SchemaModeling viral coevolution: HIV multi-clonal persistence and competition dynamics
| Authors | Franco Bagnoli, Pietro Lio', Luca Sguanci |
|---|---|
| Categories | |
| ArXiv ID | q-bio/0509006 |
| URL | https://arxiv.org/abs/q-bio/0509006 |
| DOI | 10.1016/j.physa.2005.10.055 |
| Journal | Physica A 366, 333-346 (2006) |
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.
{
"annotation_id": "2417f560-27b7-4a18-a443-2ecf058f8f2f",
"date_created": "2026-03-02T18:01:31.619000Z",
"date_modified": "2026-03-02T18:01:31.619000Z",
"file_hash": "79ecf7751bfb82423510afeccad97a8ff3e1aa543ad8c91c68d7d5773392b17c",
"private": false,
"record": {
"abstract": "The coexistence of different viral strains (quasispecies) within the same\nhost are nowadays observed for a growing number of viruses, most notably HIV,\nMarburg and Ebola, but the conditions for the formation and survival of new\nstrains have not yet been understood. We present a model of HIV quasispecies\ncompetition, that describes the conditions of viral quasispecies coexistence\nunder different immune system conditions. Our model incorporates both T and B\ncells responses, and we show that the role of B cells is important and additive\nto that of T cells. Simulations of coinfection (simultaneous infection) and\nsuperinfection (delayed secondary infection) scenarios in the early stages\n(days) and in the late stages of the infection (years) are in agreement with\nemerging molecular biology findings. The immune response induces a competition\namong similar phenotypes, leading to differentiation (quasi-speciation), escape\ndynamics and complex oscillations of viral strain abundance. We found that the\nquasispecies dynamics after superinfection or coinfection has time scales of\nseveral months and becomes even slower when the immune system response is weak.\nOur model represents a general framework to study the speed and distribution of\nHIV quasispecies during disease progression, vaccination and therapy.",
"arxiv_id": "q-bio/0509006",
"authors": [
"Franco Bagnoli",
"Pietro Lio\u0027",
"Luca Sguanci"
],
"categories": [
"q-bio.PE"
],
"doi": "10.1016/j.physa.2005.10.055",
"journal_ref": "Physica A 366, 333-346 (2006)",
"title": "Modeling viral coevolution: HIV multi-clonal persistence and competition dynamics",
"url": "https://arxiv.org/abs/q-bio/0509006"
},
"schema_id": "dorsal/arxiv",
"source": {
"execution_id": "5f63a4ab-c71d-4b8e-8bc5-5abafebbb75d",
"id": "arXiv Dataset IDs",
"type": "Model",
"variant": "snapshot-2026-03-01",
"version": "0.1.0"
},
"user_id": 1000002
}