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本文引用的文献

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Evidence for Viral Interference and Cross-reactive Protective Immunity Between Influenza B Virus Lineages.证据表明乙型流感病毒谱系之间存在病毒干扰和交叉反应性保护免疫。
J Infect Dis. 2018 Jan 30;217(4):548-559. doi: 10.1093/infdis/jix509.
2
Pathogenesis, Humoral Immune Responses, and Transmission between Cohoused Animals in a Ferret Model of Human Respiratory Syncytial Virus Infection.在雪貂人呼吸道合胞病毒感染模型中,同居动物之间的发病机制、体液免疫反应和传播。
J Virol. 2018 Jan 30;92(4). doi: 10.1128/JVI.01322-17. Print 2018 Feb 15.
3
Modelling cross-reactivity and memory in the cellular adaptive immune response to influenza infection in the host.宿主对流感感染的细胞适应性免疫反应中交叉反应性和记忆的建模。
J Theor Biol. 2017 Jan 21;413:34-49. doi: 10.1016/j.jtbi.2016.11.008. Epub 2016 Nov 15.
4
Ferrets as a Novel Animal Model for Studying Human Respiratory Syncytial Virus Infections in Immunocompetent and Immunocompromised Hosts.雪貂作为一种用于研究免疫功能正常和免疫功能低下宿主中人类呼吸道合胞病毒感染的新型动物模型。
Viruses. 2016 Jun 14;8(6):168. doi: 10.3390/v8060168.
5
Characterization of the Localized Immune Response in the Respiratory Tract of Ferrets following Infection with Influenza A and B Viruses.甲型和乙型流感病毒感染后雪貂呼吸道局部免疫反应的特征
J Virol. 2015 Dec 30;90(6):2838-48. doi: 10.1128/JVI.02797-15.
6
Viral Interference and Persistence in Mosquito-Borne Flaviviruses.蚊媒黄病毒中的病毒干扰和持续存在。
J Immunol Res. 2015;2015:873404. doi: 10.1155/2015/873404. Epub 2015 Oct 25.
7
Interference between respiratory syncytial virus and rhinovirus in respiratory tract infections in children.呼吸道合胞病毒和鼻病毒在儿童呼吸道感染中的相互干扰。
Clin Microbiol Infect. 2016 Feb;22(2):208.e1-208.e6. doi: 10.1016/j.cmi.2015.10.002. Epub 2015 Oct 16.
8
Early occurrence of influenza A epidemics coincided with changes in occurrence of other respiratory virus infections.甲型流感疫情的早期出现与其他呼吸道病毒感染发生率的变化同时发生。
Influenza Other Respir Viruses. 2016 Jan;10(1):14-26. doi: 10.1111/irv.12348.
9
Innate Immunity and the Inter-exposure Interval Determine the Dynamics of Secondary Influenza Virus Infection and Explain Observed Viral Hierarchies.先天免疫和暴露间隔决定了二次流感病毒感染的动态变化,并解释了观察到的病毒层级关系。
PLoS Comput Biol. 2015 Aug 18;11(8):e1004334. doi: 10.1371/journal.pcbi.1004334. eCollection 2015 Aug.
10
Interval Between Infections and Viral Hierarchy Are Determinants of Viral Interference Following Influenza Virus Infection in a Ferret Model.感染间隔和病毒层级是雪貂模型中流感病毒感染后病毒干扰的决定因素。
J Infect Dis. 2015 Dec 1;212(11):1701-10. doi: 10.1093/infdis/jiv260. Epub 2015 May 5.

在感染雪貂模型中研究甲型流感病毒和人类呼吸道合胞病毒之间的病毒干扰。

Investigating Viral Interference Between Influenza A Virus and Human Respiratory Syncytial Virus in a Ferret Model of Infection.

机构信息

WHO Collaborating Centre for Reference and Research on Influenza, The University of Melbourne, Melbourne.

Department of Virology, Institute of Experimental Medicine, Saint Petersburg, Russia.

出版信息

J Infect Dis. 2018 Jul 2;218(3):406-417. doi: 10.1093/infdis/jiy184.

DOI:10.1093/infdis/jiy184
PMID:29746640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7107400/
Abstract

Epidemiological studies have observed that the seasonal peak incidence of influenza virus infection is sometimes separate from the peak incidence of human respiratory syncytial virus (hRSV) infection, with the peak incidence of hRSV infection delayed. This is proposed to be due to viral interference, whereby infection with one virus prevents or delays infection with a different virus. We investigated viral interference between hRSV and 2009 pandemic influenza A(H1N1) virus (A[H1N1]pdm09) in the ferret model. Infection with A(H1N1)pdm09 prevented subsequent infection with hRSV. Infection with hRSV reduced morbidity attributed to infection with A(H1N1)pdm09 but not infection, even when an increased inoculum dose of hRSV was used. Notably, infection with A(H1N1)pdm09 induced higher levels of proinflammatory cytokines, chemokines, and immune mediators in the ferret than hRSV. Minimal cross-reactive serological responses or interferon γ-expressing cells were induced by either virus ≥14 days after infection. These data indicate that antigen-independent mechanisms may drive viral interference between unrelated respiratory viruses that can limit subsequent infection or disease.

摘要

流行病学研究观察到,流感病毒感染的季节性高峰发病时间有时与人类呼吸道合胞病毒(hRSV)感染的高峰发病时间不同,hRSV 感染的高峰发病时间延迟。这被认为是由于病毒干扰,即一种病毒的感染可以预防或延迟另一种病毒的感染。我们在雪貂模型中研究了 hRSV 和 2009 年大流行性流感 A(H1N1)病毒(A[H1N1]pdm09)之间的病毒干扰。A(H1N1)pdm09 的感染可预防随后的 hRSV 感染。hRSV 的感染降低了归因于 A(H1N1)pdm09 感染的发病率,但不能降低感染率,即使使用了更高剂量的 hRSV 接种物。值得注意的是,与 hRSV 相比,A(H1N1)pdm09 在雪貂中诱导更高水平的促炎细胞因子、趋化因子和免疫介质。感染后至少 14 天,两种病毒均未诱导出具有交叉反应性的血清学反应或干扰素 γ 表达细胞。这些数据表明,非抗原依赖性机制可能驱动不相关的呼吸道病毒之间的病毒干扰,从而限制随后的感染或疾病。