TY - JOUR
T1 - Innate antiviral cytokine response to swine influenza virus by swine respiratory epithelial cells
AU - Bakre, Abhijeet A.
AU - Jones, Les P.
AU - Murray, Jackelyn
AU - Reneer, Z. Beau
AU - Meliopoulos, Victoria A.
AU - Cherry, Sean
AU - Schultz-Cherry, Stacey
AU - Tripp, Ralph A.
N1 - Funding Information:
We acknowledge funding in part from NIAID CEIRS contract numbers HHSN2662007000006C and HHSN272204000004C to R.A.T. and funding from the Georgia Research Alliance to R.A.T. Funding for S.S.C. was provided by NIAID CEIRS contract HHSN272201400006C and by ALSAC.
Publisher Copyright:
Copyright © 2021 American Society for Microbiology. All Rights Reserved.
PY - 2021/7
Y1 - 2021/7
N2 - Swine influenza virus (SIV) can cause respiratory illness in swine. Swine contribute to influenza virus reassortment, as avian, human, and/or swine influenza viruses can infect swine and reassort, and new viruses can emerge. Thus, it is important to determine the host antiviral responses that affect SIV replication. In this study, we examined the innate antiviral cytokine response to SIV by swine respiratory epithelial cells, focusing on the expression of interferon (IFN) and interferon-stimulated genes (ISGs). Both primary and transformed swine nasal and tracheal respiratory epithelial cells were examined following infection with field isolates. The results show that IFN and ISG expression is maximal at 12 h postinfection (hpi) and is dependent on cell type and virus genotype. IMPORTANCE Swine are considered intermediate hosts that have facilitated influenza virus reassortment events that have given rise pandemics or genetically related viruses have become established in swine. In this study, we examine the innate antiviral response to swine influenza virus in primary and immortalized swine nasal and tracheal epithelial cells, and show virus strain- and host cell type-dependent differential expression of key interferons and interferon-stimulated genes.
AB - Swine influenza virus (SIV) can cause respiratory illness in swine. Swine contribute to influenza virus reassortment, as avian, human, and/or swine influenza viruses can infect swine and reassort, and new viruses can emerge. Thus, it is important to determine the host antiviral responses that affect SIV replication. In this study, we examined the innate antiviral cytokine response to SIV by swine respiratory epithelial cells, focusing on the expression of interferon (IFN) and interferon-stimulated genes (ISGs). Both primary and transformed swine nasal and tracheal respiratory epithelial cells were examined following infection with field isolates. The results show that IFN and ISG expression is maximal at 12 h postinfection (hpi) and is dependent on cell type and virus genotype. IMPORTANCE Swine are considered intermediate hosts that have facilitated influenza virus reassortment events that have given rise pandemics or genetically related viruses have become established in swine. In this study, we examine the innate antiviral response to swine influenza virus in primary and immortalized swine nasal and tracheal epithelial cells, and show virus strain- and host cell type-dependent differential expression of key interferons and interferon-stimulated genes.
KW - Interferon-stimulated gene
KW - Interferons
KW - Swine influenza virus
KW - Swine nasal cells
KW - Swine tracheal cells
UR - http://www.scopus.com/inward/record.url?scp=85109766886&partnerID=8YFLogxK
U2 - 10.1128/JVI.00692-21
DO - 10.1128/JVI.00692-21
M3 - Article
C2 - 33980596
AN - SCOPUS:85109766886
SN - 0022-538X
VL - 95
SP - 1
EP - 14
JO - Journal of Virology
JF - Journal of Virology
IS - 15
M1 - e00692-21
ER -