Pathogenesis of swine influenza virus (Thai isolates) in weanling pigs: an experimental trial.
Pathogenesis of swine influenza virus (Thai isolates) in weanling pigs: an experimental trial.
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DOI：
10.1186/1743-422x-6-34
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发表时间：
2009-03-25
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：
Sreta D;Kedkovid R;Tuamsang S;Kitikoon P;Thanawongnuwech R
本研究的目的是调查猪流感病毒（SIV）亚型H1N1和H3 N2（泰国分离株）在22日龄SPF猪中的发病机制。研究发现，感染组中的所有猪在感染后1-4天（dpi）出现典型的流感样症状体征。H1N1感染猪的肺部病变评分高于H3 N2感染猪。在两个感染组中均存在与猪流感诱导的病变相关的组织学病变，包括上皮细胞损伤、气道堵塞以及支气管周围和血管周围单核细胞浸润。免疫荧光和免疫组化使用核蛋白特异性单克隆抗体显示阳性染色细胞在2和4 dpi的两个感染组的肺切片。RT-PCR和病毒分离证实，在感染后2 dpi时，从两个感染组中均检测到病毒脱落。结果表明，这两种亚型的SIV都能引起断奶仔猪的流感样症状和肺部病变。然而，H1N1感染猪的肺部病变（肉眼和显微镜下病变）的疾病严重程度更高。系统发育分析表明，泰国H1N1亚型血凝素基因与经典的H1 SIV序列聚在一起，神经氨酸酶基因与禽源性病毒聚在一起，而H3 N2亚型血凝素基因和神经氨酸酶基因与20世纪70年代的H3 N2类人SIV聚在一起。
The objective of this study is to investigate the pathogenesis of swine influenza virus (SIV) subtype H1N1 and H3N2 (Thai isolates) in 22-day-old SPF pigs. The study found that all pigs in the infected groups developed typical signs of flu-like symptoms on 1–4 days post- infection (dpi). The H1N1-infected pigs had greater lung lesion scores than those of the H3N2-infected pigs. Histopathological lesions related to swine influenza-induced lesions consisting of epithelial cells damage, airway plugging and peribronchial and perivascular mononuclear cell infiltration were present in both infected groups. Immunofluorescence and immunohistochemistry using nucleoprotein specific monoclonal antibodies revealed positive staining cells in lung sections of both infected groups at 2 and 4 dpi. Virus shedding was detected at 2 dpi from both infected groups as demonstrated by RT-PCR and virus isolation. The results demonstrated that both SIV subtypes were able to induce flu-like symptoms and lung lesions in weanling pigs. However the severity of the diseases with regards to lung lesions both gross and microscopic lesions was greater in the H1N1-infected pigs. Based on phylogenetic analysis, haemagglutinin gene of subtype H1N1 from Thailand clustered with the classical H1 SIV sequences and neuraminidase gene clustered with virus of avian origin, whereas, both genes of H3N2 subtype clustered with H3N2 human-like SIV from the 1970s.