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Erschienen in: Archives of Virology 2/2013

01.02.2013 | Original Article

Adoptive transfer of macrophages from adult mice reduces mortality in mice infected with human enterovirus 71

verfasst von: Jiangning Liu, Xiaoying Li, Xiaoxu Fan, Chunmei Ma, Chuan Qin, Lianfeng Zhang

Erschienen in: Archives of Virology | Ausgabe 2/2013

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Abstract

Human enterovirus 71 (EV71) causes hand, foot and mouth disease in children under 6 years of age, and the neurological complications of this virus can lead to death. Until now, no vaccines or drugs have been available for the clinical control of this epidemic. Macrophages can engulf pathogens and mediate a series of host immune responses that play a role in the defence against infectious diseases. Using immunohistochemistry, we observed the localizations of virus in muscle tissues of EV71-infected mice. The macrophages isolated from the adult mice could kill the virus gradually in vitro, as shown using quantitative real-time PCR (qRT-PCR) and virus titration. Co-localisation of lysosomes and virus within macrophages suggested that the lysosomes were possibly responsible for the phagocytosis of EV71. Activation of the macrophages in the peritoneal cavity of mice four days pre-infection reduced the mortality of mice upon lethal EV71 infection. The adoptive transfer of macrophages from adult mice inhibited virus replication in the muscle tissues of infected mice, and this was followed by a relief of symptoms and a significant reduction of mortality, which suggested that the adoptive transfer of macrophages from adult humans represents a potential strategy to treat EV71-infected patients.
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Metadaten
Titel
Adoptive transfer of macrophages from adult mice reduces mortality in mice infected with human enterovirus 71
verfasst von
Jiangning Liu
Xiaoying Li
Xiaoxu Fan
Chunmei Ma
Chuan Qin
Lianfeng Zhang
Publikationsdatum
01.02.2013
Verlag
Springer Vienna
Erschienen in
Archives of Virology / Ausgabe 2/2013
Print ISSN: 0304-8608
Elektronische ISSN: 1432-8798
DOI
https://doi.org/10.1007/s00705-012-1495-4

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