Shanghai Key Laboratory of Veterinary Biotechnology, Key Laboratory of Urban Agriculture (South), Ministry of Agriculture, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai, 200240, China.
Shanghai Key Laboratory of Veterinary Biotechnology, Key Laboratory of Urban Agriculture (South), Ministry of Agriculture, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai, 200240, China.
Vet Microbiol. 2021 Jul;258:109071. doi: 10.1016/j.vetmic.2021.109071. Epub 2021 Apr 11.
The synergism of the influenza virus and respiratory tract pathogens is known to exacerbate diseases in both humans and animals. The mechanism of the co-infection of associated respiratory tract pathogens is explored in this study. Co-infection has a directional effect when influenza virus or other pathogens occur in a different order. In the present study, we used a mouse animal model to study the synergism of influenza virus and Streptococcus suis co-infection in different orders of administration. We found that the group infected with bacteria alone did not show any clinical symptoms, but the group infected with the virus alone showed 100 % mortality and clinical signs typical in infected mice. In the bacteria infected following virus pre-exposure group, the mice died before the virus-infected group and showed severer clinical signs. When the influenza virus was administered after the bacteria, the infected mice showed reduced mortality compared with mice administered the influenza virus alone. The results indicated that the order of infection significantly affected the outcome of the co-infection of these two pathogens in the mice. However, the underlying mechanism was unclear. Therefore, a transcriptome analysis of mouse lungs was conducted to explore the potential mechanism. The results showed that inflammation and cell damage signaling pathways were upregulated, which may have contributed to the increased mortality in the secondary bacterial infection group. Upregulated innate immunity may have been a major cause of reduced mortality when the bacteria were inoculated before the virus infection.
流感病毒和呼吸道病原体的协同作用已知会加重人类和动物的疾病。本研究探讨了相关呼吸道病原体共同感染的机制。当流感病毒或其他病原体以不同的顺序发生时,共同感染具有定向效应。在本研究中,我们使用小鼠动物模型研究了流感病毒和猪链球菌在不同给药顺序下的协同感染。我们发现单独感染细菌的组没有表现出任何临床症状,但单独感染病毒的组表现出 100%的死亡率和感染小鼠的典型临床症状。在病毒预先暴露后感染细菌的组中,小鼠在病毒感染组之前死亡,并表现出更严重的临床症状。当流感病毒在细菌感染后给予时,与单独给予流感病毒的小鼠相比,感染小鼠的死亡率降低。结果表明,感染顺序显著影响了这两种病原体在小鼠中的共同感染的结果。然而,其潜在机制尚不清楚。因此,对小鼠肺部进行了转录组分析,以探讨潜在的机制。结果表明,炎症和细胞损伤信号通路被上调,这可能导致继发细菌感染组死亡率增加。上调的先天免疫可能是在病毒感染前接种细菌时降低死亡率的主要原因。