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Co-immunoprecipitation of the Mouse Mx1 Protein with the Influenza A Virus Nucleoprotein
Published on: April 21, 2015
Influenza virus pathophysiology and brain invasion in mice with functional and dysfunctional Mx1 genes
Nicole R Hodgson1, Stewart G Bohnet, Jeannine A Majde
1Sleep and Performance Research Center, WWAMI Medical Education Program, Washington State University, Spokane, WA 99210-1495, United States.
Abstract:
Mice with a dysfunctional myxovirus resistance-1 (dMx1) gene transport intranasally-instilled PR8 influenza virus to the olfactory bulb (OB) within 4 h post-infection. To determine if the presence of a functional Mx1 (fMx1) gene would influence this brain viral localization and/or disease, we infected mature C57BL/6 dMx1 and fMx1 mice under the same conditions and observed sickness behaviors, viral nucleoprotein (NP) RNA expression and innate immune mediator (IIM) mRNA expression in selected tissues at 15 and 96 h post-infection. Virus invaded the OB and lungs comparably in both sub-strains at 15 and 96 h as determined by nested PCR. In contrast, virus was present in blood and somatosensory cortex of dMx1, but not fMx1 mice at 96 h. At 15 h, sickness behaviors were comparable in both sub-strains. By 96 h dMx1, but not fMx1, were moribund. In both 15 and 96 h lungs, viral NP was significantly elevated in the dMx1 mice compared to the fMx1 mice, as determined by quantitative PCR. OB expression of most IIM mRNAs was similar at both time periods in both sub-strains. In contrast, lung IIM mRNAs were elevated in fMx1 at 15 h, but by 96 h were consistently reduced compared to dMx1 mice. In conclusion, functional Mx1 did not alter OB invasion by virus but attenuated illness compared to dMx1 mice. Inflammation was similar in OBs and lungs of both strains at 15 h but by 96 h it was suppressed in lungs, but not in OBs, of fMx1 mice.
Insights
Mice with a functional Mx1 gene showed reduced influenza virus illness and spread to the brain compared to those with a dysfunctional Mx1 gene. The functional Mx1 gene attenuated disease severity and viral load in the lungs.
Area of Science:
- Virology
- Immunology
- Neuroscience
Background:
- The myxovirus resistance-1 (Mx1) gene plays a role in innate immunity against influenza viruses.
- Understanding Mx1's role in brain viral invasion and disease pathogenesis is crucial.
Purpose of the Study:
- To investigate the influence of a functional Mx1 (fMx1) gene on influenza virus localization to the olfactory bulb and subsequent disease progression.
- To compare viral spread, sickness behaviors, and immune responses in mice with dysfunctional Mx1 (dMx1) and fMx1 genes.
Main Methods:
- Intranasal instillation of PR8 influenza virus in C57BL/6 dMx1 and fMx1 mice.
- Assessment of viral nucleoprotein (NP) RNA expression via nested and quantitative PCR.
- Monitoring of sickness behaviors and innate immune mediator (IIM) mRNA expression at 15 and 96 hours post-infection.
Main Results:
- Virus invaded the olfactory bulb and lungs comparably in both groups.
- dMx1 mice showed virus in blood and somatosensory cortex, unlike fMx1 mice, by 96 hours.
- dMx1 mice exhibited moribundity and elevated lung viral NP by 96 hours, while fMx1 mice showed attenuated illness.
- Lung innate immune mediator mRNA was initially elevated in fMx1 mice but suppressed by 96 hours compared to dMx1 mice.
Conclusions:
- Functional Mx1 did not prevent olfactory bulb invasion but significantly attenuated influenza-induced illness and systemic viral spread.
- Mx1 influences disease severity and immune responses in the lungs, with suppressed inflammation in fMx1 mice by 96 hours post-infection.
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