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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Venezuelan encephalitis emergence mediated by a phylogenetically predicted viral mutation
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Venezuelan encephalitis emergence mediated by a phylogenetically predicted viral mutation

机译：系统发育预测的病毒突变介导的委内瑞拉脑炎的出现

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摘要

RNA viruses are notorious for their genetic plasticity and propensity to exploit new host-range opportunities, which can lead to the emergence of human disease epidemics such as severe acute respiratory syndrome, AIDS, dengue, and influenza. However, the mechanisms of host-range change involved in most of these viral emergences, particularly the genetic mechanisms of adaptation to new hosts, remain poorly understood. We studied the emergence of Venezuelan equine encephalitis virus (VEEV), an alphavirus pathogen of people and equines that has had severe health and economic effects in the Americas since the early 20th century. Between epidemics, VEE disappears for periods up to decades, and the viral source of outbreaks has remained enigmatic. Combined with phylogenetic analyses to predict mutations associated with a 1992-1993 epidemic, we used reverse genetic studies to identify an envelope glycoprotein gene mutation that mediated emergence. This mutation allowed an enzootic, equine-avirulent VEEV strain, which circulates among rodents in nearby forests to adapt for equine amplification. RNA viruses including alphaviruses exhibit high mutation frequencies. Therefore, ecological and epidemiological factors probably constrain the frequency of VEE epidemics more than the generation, via mutation, of amplification-competent (high equine viremia) virus strains. These results underscore the ability of RNA viruses to alter their host range, virulence, and epidemic potential via minor genetic changes. VEE also demonstrates the unpredictable risks to human health of anthropogenic changes such as the introduction of equines and humans into habitats that harbor zoonotic RNA viruses.
机译：RNA病毒以其遗传可塑性和利用新的宿主范围机会的能力而臭名昭著，这可能导致人类疾病流行病的出现，例如严重的急性呼吸道综合症，艾滋病，登革热和流感。然而，大多数这些病毒出现中所涉及的宿主范围变化的机制，特别是适应新宿主的遗传机制，仍然知之甚少。我们研究了委内瑞拉马脑炎病毒（VEEV）的出现，该病毒是人和马的甲型病毒病原体，自20世纪初以来在美洲已对健康和经济产生了严重影响。在流行病之间，VEE消失长达数十年之久，而且病毒爆发的病毒来源仍然是个谜。结合系统发育分析预测与1992-1993年流行病相关的突变，我们使用反向遗传学研究鉴定了介导出现的包膜糖蛋白基因突变。这种突变允许产生一种对动物无害的兽性VEEV株，该株在附近森林的啮齿动物中循环传播，以适应马的扩增。包括alpha病毒在内的RNA病毒具有很高的突变频率。因此，生态和流行病学因素对VEE流行病的抑制作用可能比通过扩增具有扩增能力的（高马病毒血症）病毒株的发生更受限制。这些结果强调了RNA病毒通过微小的遗传变化来改变其宿主范围，毒力和流行潜力的能力。 VEE还证明了人为改变（例如将马和人类引入带有人畜共患RNA病毒的栖息地）对人类健康的不可预测的风险。

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