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Influenza A Virus Studies in a Mouse Model of Infection
Published on: September 7, 2017
Punta Toro virus (Bunyaviridae, Phlebovirus) infection in mice: strain differences in pathogenesis and host
Michelle Mendenhall1, Min-Hui Wong, Ramona Skirpstunas
1Institute for Antiviral Research, Utah State University, Logan, UT 84322-5600, USA.
Abstract:
The Adames strain of Punta Toro virus (PTV-A, Bunyaviridae, Phlebovirus) causes an acute lethal disease in hamsters and mice. The Balliet strain of the virus (PTV-B) is generally considered to be avirulent. The difference in hamster susceptibility is likely due to the ability of PTV-A to suppress interferon (IFN)-beta similarly to that described for Rift Valley fever virus. Here we investigated strain differences in PTV pathogenesis and the IFN response in mice. Although PTV-B infection in mice did not induce systemic IFN-beta release, primary macrophages produced dramatically higher levels when exposed to the virus in culture. The importance of IFN in resistance to PTV infection was borne out in studies employing STAT-1 knock-out mice. Also, a number of genes specific to IFN response pathways were upregulated in PTV-B-infected macrophages. Our findings provide new insights into the type I IFN response during PTV infection in the mouse model of phleboviral disease.
Insights
Punta Toro virus strains show different disease severity in mice. The virulent strain suppresses interferon-beta, while the less virulent strain activates immune responses in macrophages, highlighting interferon
Area of Science:
- Virology
- Immunology
- Infectious Diseases
Background:
- Punta Toro virus (PTV) exhibits strain-specific pathogenicity, with PTV-A causing lethal disease and PTV-B being generally avirulent.
- PTV-A's virulence may stem from its ability to suppress interferon-beta (IFN-β), a mechanism seen in other phleboviruses like Rift Valley fever virus.
Purpose of the Study:
- To investigate the differences in PTV pathogenesis between strains PTV-A and PTV-B in a mouse model.
- To elucidate the role of the type I interferon (IFN) response in PTV infection and resistance.
Main Methods:
- Comparative analysis of PTV-A and PTV-B infection in mice.
- In vitro culture of primary macrophages exposed to PTV strains.
- Assessment of IFN-beta release and gene expression in infected cells and tissues.
- Studies utilizing STAT-1 knock-out mice to evaluate IFN importance.
Main Results:
- PTV-B infection in mice did not induce systemic IFN-beta release, contrasting with the known effects of PTV-A.
- Primary macrophages infected with PTV-B in culture produced significantly higher levels of IFN-beta.
- STAT-1 knock-out mice demonstrated the critical role of IFN in resistance to PTV infection.
- Genes involved in IFN response pathways were upregulated in PTV-B-infected macrophages.
Conclusions:
- Strain-specific differences in PTV pathogenesis are linked to the host's type I interferon response.
- Macrophages play a key role in mounting an IFN-beta response against PTV infection.
- Understanding the IFN response to PTV provides insights into phleboviral disease mechanisms.
