The PB2, PA, HA, NP, and NS genes of a highly pathogenic avian influenza virus A/whooper swan/Mongolia/3/2005 (H5N1) are responsible for pathogenicity in ducks.

The PB2, PA, HA, NP, and NS genes of a highly pathogenic avian influenza virus A/whooper swan/Mongolia/3/2005 (H5N1) are responsible for pathogenicity in ducks.
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高致病性禽流感病毒 A/大天鹅/蒙古/3/2005 (H5N1) 的 PB2、PA、HA、NP 和 NS 基因对鸭子具有致病性。

DOI:
10.1186/1743-422x-10-45
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发表时间:
2013-02-02
期刊:
影响因子:
4.8
通讯作者:
Kida H
Kida H
中科院分区:
医学3区
文献类型:
--
作者:
Kajihara M;Sakoda Y;Soda K;Minari K;Okamatsu M;Takada A;Kida H

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野鸭是甲型流感病毒的天然宿主。因此,鸭流感被认为是甲型流感病毒(包括鸡体内的高致病性禽流感病毒)的隐性感染。事实上,实验感染HPAIV毒株A/Hong Kong/483/1997 (H5N1) (HK483)的鸭子没有表现出任何临床症状。然而,从一只死天鹅中分离出的另一种HPAIV毒株A/大天鹅/蒙古/3/2005 (H5N1) (MON3)引起了鸭子的神经功能障碍和死亡。为了了解MON3在鸭中表现出高致病性的机制,我们比较了HK483、MON3和这两种H5N1病毒之间产生的24个重组体对家鸭的致病性。携带HK483的PB2、NP或NS基因片段的MON3单基因重组体感染的鸭无一死亡,而携带HK483的PB2、NP或NS基因片段的HK483单基因重组体在鸭中不具有致病性,这表明多基因片段参与了MON3在鸭中的致病性。所有感染了带有MON3的PB2、PA、HA、NP和NS基因片段的重组鸭在接种后5天内死亡,感染MON3的鸭也一样。接种三天后,对每种病毒在鸭体内的复制情况进行了评估。在所有检查的鸭组织中都发现了MON3和多基因重组致病性,并在脑和肺中以高滴度复制。上述结果表明,多基因因素对鸭体内MON3的高效复制起着重要作用。特别是,病毒在大脑中的生长可能与神经功能障碍和疾病严重程度有关。
Wild ducks are the natural hosts of influenza A viruses. Duck influenza, therefore, has been believed inapparent infection with influenza A viruses, including highly pathogenic avian influenza viruses (HPAIVs) in chickens. In fact, ducks experimentally infected with an HPAIV strain, A/Hong Kong/483/1997 (H5N1) (HK483), did not show any clinical signs. Another HPAIV strain, A/whooper swan/Mongolia/3/2005 (H5N1) (MON3) isolated from a dead swan, however, caused neurological dysfunction and death in ducks. To understand the mechanism whereby MON3 shows high pathogenicity in ducks, HK483, MON3, and twenty-four reassortants generated between these two H5N1 viruses were compared for their pathogenicity in domestic ducks. None of the ducks infected with MON3-based single-gene reassortants bearing the PB2, NP, or NS gene segment of HK483 died, and HK483-based single-gene reassortants bearing PB2, NP, or NS genes of MON3 were not pathogenic in ducks, suggesting that multiple gene segments contribute to the pathogenicity of MON3 in ducks. All the ducks infected with the reassortant bearing PB2, PA, HA, NP, and NS gene segments of MON3 died within five days post-inoculation, as did those infected with MON3. Each of the viruses was assessed for replication in ducks three days post-inoculation. MON3 and multi-gene reassortants pathogenic in ducks were recovered from all of the tissues examined and replicated with high titers in the brains and lungs. The present results indicate that multigenic factors are responsible for efficient replication of MON3 in ducks. In particular, virus growth in the brain might correlate with neurological dysfunction and the disease severity.