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Published on: November 1, 2011
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Innate Immune Basis for Rift Valley Fever Susceptibility in Mouse Models
Rashida Lathan1,2, Dominique Simon-Chazottes1,2, Grégory Jouvion3
1Department of Developmental & Stem Cell Biology, Unit of Mouse Functional Genetics, Institut Pasteur, F-75015, Paris, France.
Scientific Reports
|August 4, 2017
Summary
Rift Valley fever virus (RVFV) susceptibility varies between mouse strains due to immune response differences. MBT/Pas mice show early inflammation but fail to control viral load, unlike resistant BALB/cByJ mice.
Area of Science:
- Immunology
- Virology
- Genetics
Background:
- Rift Valley fever virus (RVFV) causes variable disease severity in hosts.
- Host immune responses significantly influence RVFV disease outcome.
- MBT/Pas mice exhibit extreme susceptibility, while BALB/cByJ mice show resistance.
Purpose of the Study:
- To investigate the immunological basis for differential RVFV susceptibility between MBT/Pas and BALB/cByJ mice.
- To identify key immune mechanisms contributing to RVFV pathogenesis and host survival.
Main Methods:
- Comparative analysis of immune cell populations (neutrophils, leukocytes) in infected mice.
- Measurement of serum cytokine levels, including interferon-alpha (IFN-α).
- Assessment of leukocyte expression of type I IFN receptor subunit 1 (IFNAR1) and interferon-gamma (IFN-γ) production.
Main Results:
- Lower neutrophil levels in MBT/Pas mice were not linked to susceptibility.
- MBT/Pas mice displayed earlier inflammatory responses with higher IFN-α but failed to limit viral antigen load.
- Immunological differences included lower IFNAR1 expression on leukocytes, delayed activation, and reduced IFN-γ production in MBT/Pas mice.
Conclusions:
- RVFV susceptibility in mice is linked to complex immunological alterations, not solely neutrophil levels.
- Impaired type I interferon signaling and leukocyte function contribute to severe RVFV disease in susceptible mice.
- Findings align with genetic studies suggesting a complex inheritance of RVFV resistance/susceptibility.
