Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, Hokkaido, Japan.
Virol J. 2013 Feb 2;10:45. doi: 10.1186/1743-422X-10-45.
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.
野禽是甲型流感病毒的天然宿主。因此，人们认为鸭类流感是甲型流感病毒（包括高致病性禽流感病毒（HPAIV））的隐性感染。事实上，实验感染 HPAIV 株 A/Hong Kong/483/1997（H5N1）（HK483）的鸭并未表现出任何临床症状。然而，从死天鹅中分离出的另一种 HPAIV 株 A/whooper 天鹅/蒙古/3/2005（H5N1）（MON3），可导致鸭出现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 以及这两种 H5N1 病毒之间的 24 个重组体在本地鸭中的致病性。
感染 MON3 为基础的单基因重组体，其 PB2、NP 或 NS 基因节段来自 HK483 的鸭均未死亡，而携带 MON3 的 PB2、NP 或 NS 基因节段的 HK483 为基础的单基因重组体在鸭中也无致病性，这表明多个基因节段共同导致了 MON3 在鸭中的致病性。所有感染了携带 MON3 的 PB2、PA、HA、NP 和 NS 基因节段的重组体的鸭在接种后 5 天内死亡，感染 MON3 的鸭也死亡。在接种后 3 天，对所有病毒在鸭中进行了复制评估。从所有检查的组织中都分离出了感染 MON3 和在鸭中具有致病性的多基因重组体，并在脑中复制，其滴度很高。
本研究结果表明，多基因因素是 MON3 在鸭中高效复制的原因。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相关。
