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Distinct Roles of Interferon Alpha and Beta in Controlling Chikungunya Virus Replication and Modulating Neutrophil-Mediated Inflammation
Author(s) -
Lindsey E. Cook,
Marissa C. Locke,
Alissa R. Young,
Kristen Monte,
Matthew L. Hedberg,
Raeann M. Shimak,
Kathleen C. F. Sheehan,
Deborah J. Veis,
Michael Diamond,
Deborah J. Lenschow
Publication year - 2019
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.00841-19
Subject(s) - biology , chikungunya , virology , inflammation , beta (programming language) , viral replication , virus , alphavirus , alpha interferon , alpha (finance) , alphavirus infection , interferon type i , interferon , interferon beta , immunology , medicine , construct validity , nursing , patient satisfaction , computer science , programming language
Type I interferons (IFNs) possess a range of biological activity and protect against a number of viruses, including alphaviruses. Despite signaling through a shared receptor, there are established biochemical and functional differences among the IFN subtypes. The significance of our research is in demonstrating that IFN-α and IFN-β both have protective roles during acute chikungunya virus (CHIKV) infection but do so by distinct mechanisms. IFN-α limits CHIKV replication and dissemination, whereas IFN-β protects from CHIKV pathogenesis by limiting inflammation mediated by neutrophils. Our findings support the premise that the IFN subtypes have distinct biological activities in the antiviral response.

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