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West Ashley Library
9 a.m. – 7 p.m.
Phone: (843) 766-6635
Wando Mount Pleasant Library
9 a.m. – 8 p.m.
Phone: (843) 805-6888
Village Library
9 a.m. – 6 p.m.
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St. Paul's/Hollywood Library
9 a.m. – 8 p.m.
Phone: (843) 889-3300
Otranto Road Library
9 a.m. – 8 p.m.
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Mt. Pleasant Library
9 a.m. – 8 p.m.
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McClellanville Library
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John's Island Library
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Edgar Allan Poe/Sullivan's Island Library
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Influenza A virus lacking the effector and C terminal domains of NS1 protein induces cytokines associated with high pathogenicity in mice.
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- Author(s): TURIANOVÁ, L.; LACHOVÁ, V.; BEŇOVÁ, K.; KOSTRÁBOVÁ, A.; BETÁKOVÁ, T.
- Source:
Acta Virologica; 2020, Vol. 64 Issue 1, p78-87, 10p- Subject Terms:
- Source:
- Additional Information
- Abstract: Non-structural NS1 protein of influenza A virus counters host antiviral defences by antagonizing the interferon response. The C-terminal effector domain suppresses the host response and is associated with the pathogenicity of the virus. To better understand the regulatory role of the C-terminal domain, we used reverse genetics system to generate NS1-truncated virus (NS80) and compared the cytokine profiles in the lungs of mice infected with the NS80 mutant and with the control virus A/WSN/33 (WSN). The NS80 virus was attenuated and the viral titer in the lungs was about 25 times lower than viral titer of control A/WSN/33. Mice infected with NS80 virus exhibited more severe clinical symptoms and 2 mice died 6 days post infection. NS80 virus activated retinoic-inducible gene (RIG)-1-like receptor signaling pathway more strongly than control WSN virus and mice infected with NS80 virus exhibited a greater abundance and more diverse cytokine profile. Infection with NS80 virus induced the expression of the following factors: pro-inflammatory cytokines (IL-1α, IL-1β, TNF-α, IL-16), interferons (IFN-α and IFN-ε), chemokines (CCL2, CCL11, CXCL1, CXCL5, CXCL10, CXCL11 and CXCL13), matrix metallopeptidase 9 (MMP-9), metallopeptidase inhibitor 1 (TIMP-1), macrophage colony-stimulating factor (M-CSF), and vascular cell adhesion protein 1 (VCAM-1). All these cytokines are associated with viral pathogenicity. Our data show that attenuation of the virus should not be directly linked with pathogenicity. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Acta Virologica is the property of AEPress s.r.o. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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