Reference : In vivo modulation of the innate response to pneumovirus by type-I and -III interfero...
Scientific journals : Article
Life sciences : Microbiology
Human health sciences : Immunology & infectious disease
http://hdl.handle.net/2268/108696
In vivo modulation of the innate response to pneumovirus by type-I and -III interferon-induced Bos taurus Mx1
English
Dermine, Martin mailto [Université de Liège - ULg > Département de morphologie et pathologie > Pathologie spéciale et autopsies >]
Desmecht, Daniel mailto [Université de Liège - ULg > Département de morphologie et pathologie > Pathologie spéciale et autopsies >]
Jul-2012
Journal of Interferon & Cytokine Research
Mary Ann Liebert, Inc.
32
7
332-337
Yes (verified by ORBi)
International
1079-9907
1557-7465
Larchmont
NY
[en] interferon ; innate ; pneumovirus
[en] The respiratory syncytial virus (RSV) is a major pathogen of the human species. This pneumovirus is a prominent cause of airway morbidity in children and maintains an excessive hospitalization rate despite decades of research. As involvement of a genetic vulnerability is a possibility supported by recent data, we addressed the question of whether the Mx gene products, the typical target of which consists in single-stranded negative-polarity RNA viruses, could alter the course of pneumovirus-associated disease in vivo. Wild-type and Bos taurus Mx1-expressing transgenic FVB/J mice were inoculated with the mouse counterpart and closest phylogenetic relative of RSV, pneumonia virus of mice. Survival data and follow-up of body weight, histological scores, lung virus spread and lung viral load unequivocally showed that the viral infection was severely repressed in Mx-transgenic mice, thus suggesting that pneumoviruses belong to the antiviral spectrum of mammalian Mx GTPases. Elucidating the underlying mechanisms at the molecular level could reveal critical information for the development of new anti-RSV molecules.
Researchers ; Professionals
http://hdl.handle.net/2268/108696
also: http://hdl.handle.net/2268/137230
10.1089/jir.2011.0123

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