The innate immunity of guinea pigs against highly pathogenic avian influenza virus infection
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Kun Zhang1,2, Wei wei Xu1, Zhaowei Zhang1, Jing liu1, Jing Li3, Lijuan Sun4, Weiyang Sun1, Peirong Jiao5, Xiaoyu Sang1, Zhiguang Ren1, Zhijun Yu1, Yuanguo Li1, Na Feng1, Tiecheng Wang1, Hualei Wang1, Songtao Yang1, Yongkun Zhao1, Xuemei Zhang4, Peter R. Wilker6, WenJun Liu3, Ming Liao5, Hualan Chen7, Yuwei Gao1, Xianzhu Xia1
1Key Laboratory of Jilin Province for Zoonosis Prevention and Control, The Military Veterinary Institute, Academy of Military Medical Science of PLA, Changchun, 130122, PR China
2Philips Institute for Oral Health Research, School of Dentistry, Virginia Commonwealth University, Richmond, Virginia, 23298, USA
3CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, 100101, PR China
4Department of Influenza Vaccine, Changchun Institute of Biological Product, Changchun, 130062, PR China
5College of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, PR China
6Department of Microbiology, University of Wisconsin La Crosse, La Crosse, Wisconsin, 54601, USA
7State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, 150001, PR China
Yuwei Gao, email: firstname.lastname@example.org
Xianzhu Xia, email: email@example.com
Keywords: innate immunity, guinea pig, highly pathogenic avian influenza virus, GBP-1, RIG-I
Received: August 26, 2016 Accepted: February 27, 2017 Published: March 23, 2017
H5N1 avian influenza viruses are a major pandemic concern. In contrast to the highly virulent phenotype of H5N1 in humans and many animal models, guinea pigs do not typically display signs of severe disease in response to H5N1 virus infection. Here, proteomic and transcriptional profiling were applied to identify host factors that account for the observed attenuation of A/Tiger/Harbin/01/2002 (H5N1) virulence in guinea pigs. RIG-I and numerous interferon stimulated genes were among host proteins with altered expression in guinea pig lungs during H5N1 infection. Overexpression of RIG-I or the RIG-I adaptor protein MAVS in guinea pig cell lines inhibited H5N1 replication. Endogenous GBP-1 expression was required for RIG-I mediated inhibition of viral replication upstream of the activity of MAVS. Furthermore, we show that guinea pig complement is involved in viral clearance, the regulation of inflammation, and cellular apoptosis during influenza virus infection of guinea pigs. This work uncovers features of the guinea pig innate immune response to influenza that may render guinea pigs resistant to highly pathogenic influenza viruses.
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