Emergence of Recombinant Forms of HIV Dynamics and Scaling 英文参考文献.docVIP

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Emergence of Recombinant Forms of HIV Dynamics and Scaling 英文参考文献.doc

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Emergence of Recombinant Forms of HIV Dynamics and Scaling 英文参考文献

EmergenceofRecombinantFormsofHIV: DynamicsandScaling Gajendra W. Suryavanshi, Narendra M. Dixit* DepartmentofChemicalEngineering,IndianInstituteofScience,Bangalore,India The ability to accelerate the accumulation of favorable combinations of mutations renders recombination a potent forceunderlyingtheemergenceofformsofHIVthatescapemulti-drugtherapyandspecifichostimmuneresponses. We present a mathematical model that describes the dynamics of the emergence of recombinant forms of HIV following infection with diverse viral genomes. Mimicking recent in vitro experiments, we consider target cells simultaneouslyexposedtotwodistinct,homozygousviralpopulationsandconstructdynamicalequationsthatpredict the time evolution of populations of uninfected, singly infected, and doubly infected cells, and homozygous, heterozygous, and recombinant viruses. Model predictions capture several recent experimental observations quantitatively and provide insights into the role of recombination in HIV dynamics. From analyses of data from single-round infection experiments with our description of the probability with which recombination accumulates distinctmutationspresentonthetwogenomicstrandsinavirion,weestimatethat;8recombinationalstrandtransfer events occur on average (95% confidence interval: 6–10) during reverse transcription of HIV in T cells. Model predictionsofvirusandcelldynamicsdescribethetimeevolutionandtherelativeprevalenceofvariousinfectedcell subpopulations following the onset of infection observed experimentally. Remarkably, model predictions are in quantitative agreement with the experimental scaling relationship that the percentage of cells infected with recombinant genomes is proportional to the percentage of cells coinfected with the two genomes employed at the onsetofinfection.OurmodelthuspresentsanaccuratedescriptionoftheinfluenceofrecombinationonHIVdynamics invitro.Whendistinctionsbetweendifferentviralgenomesareignored,ourmodelreducestothestandardmodelof viraldynamics