Abstract

Avian reovirus (ARV) can induce many diseases as well as immunosuppression in chickens, severely endangering the poultry industry. Interferons (IFNs) play an antiviral role by inducing the expression of interferon-stimulated genes (ISGs). The effect of ARV infection on the expression of host ISGs is unclear. Specific-pathogen-free (SPF) chickens were infected with ARV strain S1133 in this study, and real time quantitative PCR was used to detect changes in the dynamic expression of IFNs and common ISGs in joints of SPF chickens. The results showed that the transcription levels of IFNA, IFNB, and several ISGs, including myxovirus resistance (MX), interferon-induced transmembrane protein 3 (IFITM3), protein kinase R (PKR), oligoadenylate synthase (OAS), interferon-induced protein with tetratricopeptide repeats 5 (IFIT5), interferon-stimulated gene 12 (ISG12), virus inhibitory protein (VIPERIN), interferon-alpha-inducible protein 6 (IFI6), and integrin-associated protein (CD47), were upregulated in joints on days 1–7 of infection (the levels of increase of MX, IFIT5, OAS, VIPERIN, ISG12, and IFI6 were the most significant, at hundreds-fold). In addition, the expression levels of the ISGs encoding zinc finger protein 313 (ZFP313), and DNA damage–inducible transcript 4 (DDIT4) increased suddenly on the 1st or 2nd day, then decreased to control levels. The ARV viral load in chicken joints rapidly increased after 1 day of viral challenge, and the viral load remained high within 6 days of viral challenge. The ARV viral load sharply decreased starting on day 7. These results indicate that in SPF chicken joints, many ISGs have mRNA expression patterns that are basically consistent with the viral load in joints. IFNA, IFNB, and the ISGs MX, IFITM3, PKR, OAS, IFIT5, ISG12, VIPERIN, IFI6, and CD47 play important roles in defending against ARV invasion, inhibiting ARV replication and proliferation, and promoting virus clearance. These results enrich our understanding of the innate immune response mechanisms of hosts against ARV infection and provide a theoretical basis for prevention and control of ARV infection.

Highlights

  • Avian reovirus (ARV) belongs to the genus Orthoreovirus, family Reoviridae

  • Analysis of changes in the transcriptional expression levels of interferon-stimulated genes (ISGs) after ARV infection is important to better understand the pathogenesis of ARV, and may be helpful for determining the ISGs that may be involved in the anti-viral defense against ARV

  • Our real time quantitative PCR showed that both of these type I IFNs expression were upregulated in joints of SPF chickens after ARV S1133 infection, indicating that ARV infection can upregulate IFN expression

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Summary

Introduction

Avian reovirus (ARV) belongs to the genus Orthoreovirus, family Reoviridae. It mainly causes viral arthritis, chronic respiratory diseases, reduction in egg production, and runting-stunting syndrome and causes severe immunosuppression, all of which bring great economic losses to the poultry industry [1,2,3]. Most birds appear to be infected via the fecaloral route, and through the respiratory tract and through skin lesions [4]. Histological analyses have show that, major gross pathological lesions included marked swelling, edema, and hemorrhages. Histological examination demonstrated necrosis and inflammation of muscle fibers, and mixed inflammatory infiltrate was observed in subcutaneous tissue and tendon sheaths [5, 6]

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