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Pathogenicity of the Novel A/H7N9 Influenza Virus in Mice

机译：新型A / H7N9流感病毒在小鼠中的致病性

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A novel avian-origin influenza A/H7N9 virus infecting humans was first identified in March 2013 and, as of 30?May 2013, has caused 132 human infections leading to 33 deaths. Phylogenetic studies suggest that this virus is a reassortant, with the surface hemagglutinin (HA) and neuraminidase (NA) genes being derived from duck and wild-bird viruses, respectively, while the six “internal gene segments” were derived from poultry H9N2 viruses. Here we determine the pathogenicity of a human A/Shanghai/2/2013 (Sh2/H7N9) virus in healthy adult mice in comparison with that of A/chicken/Hong Kong/HH8/2010 (ck/H9N2) virus, highly pathogenic avian influenza (HPAI) A/Hong Kong/483/1997 (483/H5N1) virus, and a duck influenza A H7N9 virus of different genetic derivation, A/duck/Jiangxi/3286/2009 (dk/H7N9). Intranasal infection of mice with Sh2/H7N9 virus doses of 103, 104, and 105?PFU led to significant weight loss without fatality. This virus was more pathogenic than dk/H7N9 and ck/H9N2 virus, which has six internal gene segments that are genetically similar to Sh2/H7N9. Sh2/H7N9 replicated well in the nasal cavity and lung, but there was no evidence of virus dissemination beyond the respiratory tract. Mice infected with Sh2/H7N9 produced higher levels of proinflammatory cytokines in the lung and serum than did ck/H9N2 and dk/H7N9 but lower levels than 483/H5N1. Cytokine induction was positively correlated with virus load in the lung at early stages of infection. Our results suggest that Sh2/H7N9 virus is able to replicate and cause disease in mice without prior adaptation but is less pathogenic than 483/H5N1 virus. >IMPORTANCE An H7N9 virus isolate causing fatal human disease was found to be more pathogenic for mice than other avian H9N2 or H7N9 viruses but less pathogenic than the highly pathogenic avian influenza virus (HPAI) H5N1. Similarly, the ability of Sh2/H7N9 to elicit proinflammatory cytokines in the lung and serum of mice was intermediate to ck/H9N2 and dk/H7N9 on the one hand and HPAI H5N1 on the other. These findings accord with the observed epidemiology in humans, in whom, as with seasonal influenza viruses, H7N9 viruses cause severe disease predominantly in older persons while HPAI H5N1 can cause severe respiratory disease and death in children and young adults.
机译：2013年3月首次发现了一种新型的禽源性A / H7N9禽流感病毒，并于2013年5月30日至5月30日感染人类，导致33人死亡。系统发育研究表明，该病毒是重组病毒，表面血凝素（HA）和神经氨酸酶（NA）基因分别来自鸭和野鸟病​​毒，而六个“内部基因片段”则来自禽H9N2病毒。在这里，我们确定人成年A / Shanghai / 2/2013（Sh2 / H7N9）病毒在健康成年小鼠中的致病性，与高致病性禽流感A /鸡/香港/ HH8 / 2010（ck / H9N2）的致病性进行比较流感（HPAI）A /香港/ 483/1997（483 / H5N1）病毒和具有不同遗传来源的鸭流感A H7N9病毒，A / duck / Jiangxi / 3286/2009（dk / H7N9）。用Sh2 / H7N9病毒剂量分别为10 3 ，10 4 和10 5 ？PFU的小鼠进行鼻内感染可导致体重减轻而无死亡。该病毒比dk / H7N9和ck / H9N2病毒更具致病性，后者具有六个内部基因区段，这些区段在基因上与Sh2 / H7N9相似。 Sh2 / H7N9在鼻腔和肺中复制良好，但没有证据表明病毒在呼吸道以外传播。与ck / H9N2和dk / H7N9相比，被Sh2 / H7N9感染的小鼠在肺和血清中产生的促炎细胞因子水平更高，但低于483 / H5N1。在感染的早期，细胞因子的诱导与肺中病毒载量呈正相关。我们的结果表明，Sh2 / H7N9病毒能够在没有事先适应的情况下在小鼠中复制并引起疾病，但其致病性低于483 / H5N1病毒。 >重要发现，导致致命人类疾病的H7N9病毒分离株对小鼠的致病性高于其他禽类H9N2或H7N9病毒，但其致病性低于高致病性禽流感病毒H5N1。类似地，Sh2 / H7N9在小鼠的肺和血清中诱发促炎细胞因子的能力一方面在ck / H9N2和dk / H7N9的中间，另一方面在HPAI H5N1的中间。这些发现与在人类中观察到的流行病学一致，在人类中，与季节性流感病毒一样，H7N9病毒主要导致老年人的严重疾病，而HPAI H5N1则可能导致儿童和年轻人的严重呼吸道疾病和死亡。

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