Journal article
Interferon type I receptor-deficient mice have altered disease symptoms in response to influenza virus
Brain, behavior, and immunity, Vol.21(3), pp.311-322
2007
Handle:
https://hdl.handle.net/2376/112269
PMCID: PMC1820588
PMID: 17098395
Abstract
The role of type I interferons (IFNs) in mediation of acute viral symptoms (fever, somnolence, anorexia, etc.) is unknown. To determine the role of type I IFN in selected symptom development, body temperature and sleep responses to a marginally lethal dose of X-31 influenza virus were examined in mice with a targeted mutation of the IFN receptor type I (IFN-RI knockouts) and compared to wild-type 129 SvEv control mice. Mice were monitored for 48
h to determine baseline temperature and sleep profiles prior to infection, and then for 9 days following infection. Hypothermic responses to virus were perceptible beginning at 64
h post-infection (PI) and were more marked in KO mice until 108
h, when hypothermia became more exaggerated in wild-type controls. Temperatures of wild-type mice continued to decline through day 9 while temperatures in IFN-RI KO mice stabilized. Time spent in non-rapid eye movement sleep (NREMS) increased in KO mice when hypothermia was marked and then returned to baseline levels, while NREMS continued to increase in wild-type mice through day 9. Other sleep parameters [time spent in rapid eye movement sleep (REMS), relative NREMS EEG slow wave activity, NREMS EEG power density] were all reduced in wild-type mice compared to KOs from days 3 to 8 while REMS low frequency EEG power density increased in wild-type relative to KOs. In conclusion, our results indicate that the presence of functional type I IFN slightly ameliorates disease symptoms early in the X-31 infection while exacerbating disease symptoms later in the infection.
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Details
- Title
- Interferon type I receptor-deficient mice have altered disease symptoms in response to influenza virus
- Creators
- Tim R TraynorJeannine A MajdeStewart G BohnetJames M Krueger
- Publication Details
- Brain, behavior, and immunity, Vol.21(3), pp.311-322
- Academic Unit
- Integrative Physiology and Neuroscience, Department of
- Publisher
- Elsevier Inc
- Identifiers
- 99900547727201842
- Language
- English
- Resource Type
- Journal article