HIV毒株的竞争网络：先来的具有“奠基者效应”

  当人类机体感染第一株HIV病毒后，该毒株就会形成一种特殊的群体以至于其在后期的HIV疫情流行中占据主导地位，近日发表在国际杂志PLoS Computational Biology上的一篇研究论文中，来自匈牙利罗兰大学(Eötvös Loránd University)的研究人员就揭示了为何全球性的HIV混合突变毒株扩散比较缓慢。

  文章中，研究者对模拟的流行病模式进行了相关分析，目的在于理解不同的HIV毒株如何在相同的人群机体中进行竞争及互相干扰。研究者Bence Ferdinandy教授表示，一旦HIV毒株建立了稳定的流行病趋势，其就会减缓第二种不同HIV毒株在人群中的入侵速度。

  首次感染HIV毒株的个体会存活相对较长的一段时间，而且感染者机体对第二种HIV毒株的二次感染就会产生反弹（并不容易感染），在性接触的社交网络中，感染个体会对入侵HIV的毒株实施有效地拦截。本研究结果指出，在当前艾滋病疫情中占据主导地位的HIV突变株或许并不是最多数传播的毒株，这些HIV毒株只是非常幸运，因为其选择了最佳的时机第一时间在人群中实施了感染及传播。

  较强的传染性毒株都更容易存活或者通过突变重新以另一种方式出现或重组，而且这些毒株的生长势头最终往往会超过当前的突变体毒株；因此研究者就提示说，当前的流行病学趋势或许并不是固定的，有可能在未来的一段时间内还会继续变化，相比较而言，消除当前HIV毒株感染的流行趋势或许还会增加在新的交叉传播感染过程中新HIV毒株谱系的出现。（转化医学网360zhyx.com）

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转化医学网推荐的原文阅读：

HIV Competition Dynamics over Sexual Networks: First Comer Advantage Conserves Founder Effects
PLoS Computational Biology DOI: 10.1371/journal.pcbi.1004093
Bence Ferdinandy,
Affiliation: Department of Biological Physics, Eötvös Loránd University, Budapest, Hungary
⨯ Enys Mones,
Affiliation: Department of Biological Physics, Eötvös Loránd University, Budapest, Hungary
⨯ Tamás Vicsek,
Affiliations: Department of Biological Physics, Eötvös Loránd University, Budapest, Hungary, MTA-ELTE Statistical and Biological Physics Research Group, Eötvös Loránd University and the Hungarian Academy of Sciences, Budapest, Hungary
⨯ Viktor Müller
Outside Africa, the global phylogeography of HIV is characterized by compartmentalized local epidemics that are typically dominated by a single subtype, which indicates strong founder effects. We hypothesized that the competition of viral strains at the epidemic level may involve an advantage of the resident strain that was the first to colonize a population. Such an effect would slow down the invasion of new strains, and thus also the diversification of the epidemic. We developed a stochastic modelling framework to simulate HIV epidemics over dynamic contact networks. We simulated epidemics in which the second strain was introduced into a population where the first strain had established a steady-state epidemic, and assessed whether, and on what time scale, the second strain was able to spread in the population. Simulations were parameterized based on empirical data; we tested scenarios with varying levels of overall prevalence. The spread of the second strain occurred on a much slower time scale compared with the initial expansion of the first strain. With strains of equal transmission efficiency, the second strain was unable to invade on a time scale relevant for the history of the HIV pandemic. To become dominant over a time scale of decades, the second strain needed considerable (>25%) advantage in transmission efficiency over the resident strain. The inhibition effect was weaker if the second strain was introduced while the first strain was still in its growth phase. We also tested how possible mechanisms of interference (inhibition of superinfection, depletion of highly connected hubs in the network, one-time acute peak of infectiousness) contribute to the inhibition effect. Our simulations confirmed a strong first comer advantage in the competition dynamics of HIV at the population level, which may explain the global phylogeography of the virus and may influence the future evolution of the pandemic.