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Inferring epidemiologic dynamics from viral evolution: 2014–2015 Eurasian/North American highly pathogenic avian influenza viruses exceed transmission threshold R0 = 1 in wild birds and poultry in North America

机译:从病毒进化中推断流行病学动态:2014-2015年欧亚/北美高致病性禽流感病毒超过传播阈值R0 = 1在北美的野生鸟类和家禽中

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摘要

Highly pathogenic avian influenza virus (HPAIV) is a multihost pathogen with lineages that pose health risks for domestic birds, wild birds, and humans. One mechanism of intercontinental HPAIV spread is through wild bird reservoirs, and wild birds were the likely sources of a Eurasian (EA) lineage HPAIV into North America in 2014. The introduction resulted in several reassortment events with North American (NA) lineage low‐pathogenic avian influenza viruses and the reassortant EA/NA H5N2 went on to cause one of the largest HPAIV poultry outbreaks in North America. We evaluated three hypotheses about novel HPAIV introduced into wild and domestic bird hosts: (i) transmission of novel HPAIVs in wild birds was restricted by mechanisms associated with highly pathogenic phenotypes; (ii) the HPAIV poultry outbreak was not self‐sustaining and required viral input from wild birds; and (iii) reassortment of the EA H5N8 generated reassortant EA/NA AIVs with a fitness advantage over fully Eurasian lineages in North American wild birds. We used a time‐rooted phylodynamic model that explicitly incorporated viral population dynamics with evolutionary dynamics to estimate the basic reproductive number (R 0) and viral migration among host types in domestic and wild birds, as well as between the EA H5N8 and EA/ style="fixed-case">NA H5N2 in wild birds. We did not find evidence to support hypothesis (i) or (ii) as our estimates of the transmission parameters suggested that the style="fixed-case">HPAIV outbreak met or exceeded the threshold for persistence in wild birds (R 0 > 1) and poultry (R 0 ≈ 1) with minimal estimated transmission among host types. There was also no evidence to support hypothesis (iii) because R 0 values were similar among style="fixed-case">EA H5N8 and style="fixed-case">EA/ style="fixed-case">NA H5N2 in wild birds. Our results suggest that this novel style="fixed-case">HPAIV and reassortments did not encounter any transmission barriers sufficient to prevent persistence when introduced to wild or domestic birds.
机译:高致病性禽流感病毒(HPAIV)是具有谱系的多宿主病原体,对家禽,野禽和人类构成健康风险。洲际HPAIV传播的一种机制是通过野生鸟类储集层,而野生鸟类是2014年进入北美洲的欧亚(EA)谱系HPAIV的可能来源。此引入导致了北美(NA)谱系低致病性的多次重组事件禽流感病毒和重组的EA / NA H5N2继续成为北美最大的HPAIV家禽暴发之一。我们评估了关于引入野生和家禽宿主中的新型HPAIV的三个假设:(i)新型HPAIV在野禽中的传播受到与高致病性表型相关的机制的限制; (ii)HPAIV家禽暴发不是自我维持的,需要野生鸟类的病毒输入; (iii)重新排列EA H5N8产生的重新排列的EA / NA AIV,在北美野生鸟类中比完全欧亚血统具有适应性优势。我们使用了根深蒂固的系统动力学模型,将病毒种群动力学与进化动力学明确结合在一起,以估算基本繁殖数(R 0)和病毒在家禽和野生禽之间以及EA H5N8和EA / <野生鸟类中的H5N2。我们没有发现支持假设(i)或(ii)的证据,因为我们对传播参数的估计表明 style =“ fixed-case”> HPAIV 爆发达到或超过了野外持久性的阈值估计在宿主类型之间传播最少的禽类(R 0> 1)和家禽(R0≈1)。也没有证据支持假设(iii),因为 style =“ fixed-case”> EA H5N8和 style =“ fixed-case”> EA 之间的R 0值相似/ style =“ fixed-case”> NA H5N2在野生鸟类中。我们的研究结果表明,这种新颖的 style =“ fixed-case”> HPAIV 和重组方法在引入野生或家禽时没有遇到足以阻止持久性的传播障碍。

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