Modeling Evolutionary Dynamics of HIV Infection
We have modelled the within-patient evolutionary process during HIV infection. We have studied viral evolution at population level (competition on the same receptor) and at species level (competitions on different receptors). During the HIV infection, several mutants of the virus arise, which are able to use different chemokine receptors, in particular the CCR5 and CXCR4 coreceptors (termed R5 and X4 phenotypes, respectively). Phylogenetic inference of chemokine receptors suggests that virus mutational pathways may generate R5 variants able to interact with a wide range of chemokine receptors different from CXCR4. Using the chemokine tree topology as conceptual framework for HIV viral speciation, we present a model of viral phenotypic mutations from R5 to X4 strains which reflect HIV late infection dynamics. Our model investigates the action of Tumor Necrosis Factor in AIDS progression and makes suggestions on better design of HAART therapy.
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