Tarasiuk Karolina, Kycko Anna, Świętoń Edyta, Bocian Łukasz, Wyrostek Krzysztof, Śmietanka Krzysztof
National Veterinary Research Institute, Department of Poultry Diseases, Al. Partyzantów 57, 24-100 Puławy, Poland.
National Veterinary Research Institute, Department of Pathology, Al. Partyzantów 57, 24-100 Puławy, Poland.
Pathogens. 2023 Jan 30;12(2):217. doi: 10.3390/pathogens12020217.
In this study, we investigated the clinical response, viral shedding, transmissibility, pathologic lesions, and tropism of HPAIV Gs/Gd H5N8 subtype (clade 2.3.4.4b), following experimental infection of three groups of captive mallards (): (i) fully susceptible, (ii) pre-exposed to low pathogenic avian influenza virus (LPAIV) H5N1 subtype, and (iii) pre-exposed to LPAIV H3N8 subtype. Infection of naïve mallards with HPAIV H5N8 resulted in ~60% mortality, neurological signs, abundant shedding, and transmission to contact ducks, who also became sick and died. High amounts of viral RNA were found in all collected organs, with the highest RNA load recorded in the brain. The IHC examinations performed on tissues collected at 4 and 14 days post-infection (dpi) revealed tropism to nervous tissue, myocardium, respiratory epithelium, and hepatic and pancreatic cells. The mallards pre-exposed to LPAIV H5N1 and challenged with HPAIV H5N8 were asymptomatic and showed a significant reduction of viral RNA shedding, yet still sufficient to cause infection (but no disease) in the contact ducks. The AIV antigen was not detected in organs at 4 and 14 dpi, and microscopic lesions were mild and scarce. Similarly, mallards previously inoculated with LPAIV H3N8 remained healthy after challenge with HPAIV H5N8, but viral RNA was detected in large quantities in swabs and organs, particularly in the early phase of infection. However, in contrast to mallards from group I, the IHC staining yielded negative results at the selected timepoints. The virus was transmitted to contact birds, which remained symptomless but demonstrated low levels of viral RNA shedding and mild- to moderate tissue damage despite negative IHC staining. The results indicate that naïve mallards are highly susceptible to HPAIV H5N8 clade 2.3.4.4b and that homo- and heterosubtypic immunity to LPAIV can mitigate the clinical outcomes of infection.
在本研究中，我们对三组圈养野鸭进行实验性感染，调查了高致病性禽流感病毒（HPAIV）Gs/Gd H5N8亚型（2.3.4.4b分支）的临床反应、病毒脱落、传播性、病理损伤和嗜性：（i）完全易感组，（ii）预先暴露于低致病性禽流感病毒（LPAIV）H5N1亚型组，以及（iii）预先暴露于LPAIV H3N8亚型组。用HPAIV H5N8感染未接触过该病毒的野鸭，导致约60%的死亡率、神经症状、大量病毒脱落，并传播给接触的鸭子，这些接触鸭也生病并死亡。在所有采集的器官中均发现大量病毒RNA，其中大脑中的RNA载量最高。在感染后4天和14天（dpi）采集的组织上进行的免疫组织化学（IHC）检查显示，该病毒对神经组织、心肌、呼吸道上皮以及肝和胰腺细胞具有嗜性。预先暴露于LPAIV H5N1并受到HPAIV H5N8攻击的野鸭无症状，病毒RNA脱落显著减少，但仍足以在接触鸭中引起感染（但无疾病）。在4天和14天dpi时，器官中未检测到禽流感病毒抗原，微观病变轻微且少见。同样，先前接种LPAIV H3N8的野鸭在受到HPAIV H5N8攻击后保持健康，但在拭子和器官中大量检测到病毒RNA，尤其是在感染早期。然而，与第一组野鸭不同，在选定的时间点，免疫组织化学染色结果为阴性。该病毒传播给接触的鸟类，这些鸟类无症状，但尽管免疫组织化学染色为阴性，仍表现出低水平的病毒RNA脱落和轻度至中度的组织损伤。结果表明，未接触过该病毒的野鸭对HPAIV H5N8 2.3.4.4b分支高度易感，并且对LPAIV的同源和异源亚型免疫可以减轻感染的临床结果。
