Experimental infection with a Thai reassortant swine influenza virus of pandemic H1N1 origin induced disease.
Experimental infection with a Thai reassortant swine influenza virus of pandemic H1N1 origin induced disease.
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DOI：
10.1186/1743-422x-10-88
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发表时间：
2013-03-16
期刊：
影响因子：
4.8
通讯作者：
Thanawongnuwech R
中科院分区：
文献类型：
--
作者：
Charoenvisal N;Keawcharoen J;Sreta D;Tantawet S;Jittimanee S;Arunorat J;Amonsin A;Thanawongnuwech R
2009年人类出现大流行性H1N1甲型流感病毒后，这种新型病毒传播到了猪群中。猪是这种病毒的潜在宿主，可以作为流感病毒基因突变的混合容器。2009年的大流行最终出现了令人讨厌的病毒，并在包括泰国在内的世界各地的猪群中报告。由于发现了这种新出现的疾病，因此对这种新型病毒进行了致病机理研究，以便制定未来猪和人类群体的疾病预防和控制措施。将从泰国猪分离的2009年H1N1大流行病毒（pH 1 N1）及其再感染病毒（rH 1 N1）接种到2个单独的9、3周龄猪群中。队列由一组实验感染pH 1 N1和一组rH 1 N1组成。还包括由3只猪组成的阴性对照组。观察并比较两组患者的临床体征、病毒脱落和病理学变化。随后，在接种后2、4和12天（DPI）对病毒接种组的3头猪和对照组的1头猪进行尸检。结果表明，感染两种病毒的猪表现出典型的流感样临床体征和不同严重程度的组织病理学病变。两组流感感染猪在1-4 DPI时均出现轻度至中度肺部体征。有趣的是，直到实验结束（12 DPI），两组猪的鼻拭子中都检测到病毒RNA。本研究表明，从自然感染的猪中分离的pH 1 N1和rH 1 N1流感病毒都会在实验接种的保育猪中诱发急性呼吸道疾病。尽管rH 1 N1感染组动物表现出更严重的临床症状，有更多的猪脱落病毒，注意到肺病变的组织病理学严重程度增加，肺组织中的病毒抗原增加，但与pH 1 N1感染组相比，这些发现没有统计学意义。有趣的是，直到实验结束，都可以从鼻拭子中检测到两种病毒的病毒遗传物质。与其他猪流感病毒相似，rH 1 N1和pH 1 N1的临床症状和病理损伤均限于呼吸道。
Following the emergence of the pandemic H1N1 influenza A virus in 2009 in humans, this novel virus spread into the swine population. Pigs represent a potential host for this virus and can serve as a mixing vessel for genetic mutations of the influenza virus. Reassortant viruses eventually emerged from the 2009 pandemic and were reported in swine populations worldwide including Thailand. As a result of the discovery of this emergent disease, pathogenesis studies of this novel virus were conducted in order that future disease protection and control measures in swine and human populations could be enacted. The pandemic H1N1 2009 virus (pH1N1) and its reassortant virus (rH1N1) isolated from pigs in Thailand were inoculated into 2 separate cohorts of 9, 3-week-old pigs. Cohorts were consisted of one group experimentally infected with pH1N1 and one group with rH1N1. A negative control group consisting of 3 pigs was also included. Clinical signs, viral shedding and pathological lesions were investigated and compared. Later, 3 pigs from viral inoculated groups and 1 pig from the control group were necropsied at 2, 4, and 12 days post inoculation (DPI). The results indicated that pigs infected with both viruses demonstrated typical flu-like clinical signs and histopathological lesions of varying severity. Influenza infected-pigs of both groups had mild to moderate pulmonary signs on 1-4 DPI. Interestingly, pigs in both groups demonstrated viral RNA detection in the nasal swabs until the end of the experiment (12 DPI). The present study demonstrated that both the pH1N1 and rH1N1 influenza viruses, isolated from naturally infected pigs, induced acute respiratory disease in experimentally inoculated nursery pigs. Although animals in the rH1N1-infected cohort demonstrated more severe clinical signs, had higher numbers of pigs shedding the virus, were noted to have increased histopathological severity of lung lesions and increased viral antigen in lung tissue, the findings were not statistically significant in comparison with the pH1N1-infected group. Interestingly, viral genetic material of both viruses could be detected from the nasal swabs until the end of the experiment. Similar to other swine influenza viruses, the clinical signs and pathological lesions in both rH1N1 and pH1N1 were limited to the respiratory tract.