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Comparison of pathogenicity of subtype H9 avian influenza wild-type viruses from a wide geographic origin expressing mono-, di-, or tri-basic hemagglutinin cleavage sites

机译:亚型H9禽流感野生型病毒的致病性与宽地理来源的致病性与表达单,二 - 或三碱基血凝素切割位点

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摘要

Abstract An intravenous pathogenicity index (IVPI) of > 1.2 in chickens or, in case of subtypes H5 and H7, expression of a polybasic hemagglutinin cleavage site (HACS), signals high pathogenicity (HP). Viruses of the H9N2-G1 lineage, which spread across Asia and Africa, are classified to be of low pathogenicity although, in the field, they became associated with severe clinical signs and epizootics in chickens. Here we report on a pre-eminent trait of recent H9N2-G1 isolates from Bangladesh and India, which express a tribasic HACS (motif PAKSKR-GLF; reminiscent of an HPAIV-like polybasic HACS) and compare their features to H9Nx viruses with di- and monobasic HACS from other phylogenetic and geographic origins. In an in vitro assay, the tribasic HACS of H9N2 was processed by furin-like proteases similar to bona fide H5 HPAIV while some dibasic sites showed increased cleavability but monobasic HACS none. Yet, all viruses remained trypsin-dependent in cell culture. In ovo, only tribasic H9N2 viruses were found to replicate in a grossly extended spectrum of embryonic organs. In contrast to all subtype H5/H7 HPAI viruses, tribasic H9N2 viruses did not replicate in endothelial cells either in the chorio-allantoic membrane or in other embryonic tissues. By IVPI, all H9Nx isolates proved to be of low pathogenicity. Pathogenicity assessment of tribasic H9N2-G1 viruses remains problematic. It cannot be excluded that the formation of a third basic amino acid in the HACS forms an intermediate step towards a gain in pathogenicity. Continued observation of the evolution of these viruses in the field is recommended.
机译:摘要鸡中> 1.2的静脉内致病性指数(IVPI),或者在亚型H5和H7的情况下,多元血凝素切割位点(HACS)的表达,发出高致病性(HP)。 H9N2-G1血统的病毒,跨越亚洲和非洲的分类,分为低致病性,尽管在该领域,它们变得与鸡中严重的临床症状和外膜引发相关。在这里,我们报告了孟加拉国和印度最近的H9N2-G1分离株的杰出特征,其表达了三次HACS(MOTIF PAKSKR-GLF;让人联想到HPAIV样的多元HACS)并将其特征与DI-与H9NX病毒进行比较和来自其他系统发育和地理起源的单卤素HACs。在体外测定中,H9N2的三胞胎HAC由类似于Bona FIDE H5 HPAIV的Furin样蛋白酶加工,而一些二元位点显示出增加的可切割性但无卤素HACS无。然而,所有病毒依赖于细胞培养物依赖胰蛋白酶。在卵o中,发现只发现胚胎H9N2病毒在胚胎器官的严重扩展光谱中复制。与所有亚型H5 / H7 HPAI病毒相比,Tribasic H9N2病毒在核心 - 腺体膜或其他胚胎组织中未在内皮细胞中复制。通过IVPI,所有H9NX分离物被证明是低致病性。致血糖H9N2-G1病毒的致病性评估仍然存在问题。不能排除在HACS中形成第三个基本氨基酸形成致病性增益的中间步骤。持续观察领域中这些病毒的演变。

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