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摘要翻译：
在HIV感染过程中，出现了几种准种，它们能够使用不同的共受体，特别是CCR5和CXCR4共受体（分别为R5和X4表型）。共受体使用的转换与疾病向艾滋病阶段的更快进展有关。随着几家制药公司开始R5和X4药物的大型III期试验，需要模型来预测病毒株的共同进化和竞争动态。我们提出了一个描述R5准种动力学的HIV早期感染模型和一个描述R5到X4转换的HIV晚期感染模型。我们报告了以下发现：重叠感染或共感染后，准种动态有几个月的时间尺度，在CD4+T细胞数量较低时，准种动态变得更慢。在艾滋病晚期，CD4+T细胞的曲线下降，可以考虑X4相关的肿瘤坏死因子动态来描述。趋化因子受体的系统发育推断表明，病毒突变途径可能产生与CXCR4不同的趋化因子受体相互作用的R5变异体。这可能解释了在艾滋病晚期观察到的免疫系统的大规模信号中断，并可能与疫苗接种和治疗有关。
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英文标题：
《Mathematical Model of HIV superinfection dynamics and R5 to X4 switch》
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作者：
Luca Sguanci, Franco Bagnoli, Pietro Lio
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最新提交年份：
2006
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分类信息：
一级分类：Quantitative Biology 数量生物学
二级分类：Populations and Evolution 种群与进化
分类描述：Population dynamics, spatio-temporal and epidemiological models, dynamic speciation, co-evolution, biodiversity, foodwebs, aging; molecular evolution and phylogeny; directed evolution; origin of life
种群动力学；时空和流行病学模型；动态物种形成；协同进化；生物多样性；食物网；老龄化；分子进化和系统发育；定向进化；生命起源
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一级分类：Quantitative Biology 数量生物学
二级分类：Other Quantitative Biology 其他定量生物学
分类描述：Work in quantitative biology that does not fit into the other q-bio classifications
不适合其他q-bio分类的定量生物学工作
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英文摘要：
During the HIV infection several quasispecies of the virus arise, which are able to use different coreceptors, in particular the CCR5 and CXCR4 coreceptors (R5 and X4 phenotypes, respectively). The switch in coreceptor usage has been correlated with a faster progression of the disease to the AIDS phase. As several pharmaceutical companies are starting large phase III trials for R5 and X4 drugs, models are needed to predict the co-evolutionary and competitive dynamics of virus strains. We present a model of HIV early infection which describes the dynamics of R5 quasispecies and a model of HIV late infection which describes the R5 to X4 switch. We report the following findings: after superinfection or coinfection, quasispecies dynamics has time scales of several months and becomes even slower at low number of CD4+ T cells. The curve of CD4+ T cells decreases, during AIDS late stage, and can be described taking into account the X4 related Tumor Necrosis Factor dynamics. Phylogenetic inference of chemokine receptors suggests that viral mutational pathway may generate R5 variants able to interact with chemokine receptors different from CXCR4. This may explain the massive signaling disruptions in the immune system observed during AIDS late stages and may have relevance for vaccination and therapy.
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PDF链接：
https://arxiv.org/pdf/q-bio/0603003
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