Abstract

In recent years, the emerging highly pathogenic avian influenza (HPAI) A(H5N8) virus has been reported with features of widely spread, an expanding host range, and cross-species transmission, attracting wide attention. The domestic duck plays a major role in the epidemiological cycle of the HPAI H5N8 virus, but little is known concerning innate immune responses during influenza infection in duck species. In this study, we used two wild-bird-origin viruses, H5N8 and H4N6, to conduct duck infection experiments, and detect the load of the two viruses, and retinoic acid-inducible gene I (RIG-I) and interferon β (IFN-β) in the host’s natural immune response. Through comparison, it is found that the expression levels of RIG-I and IFN-β are both fluctuating. The innate immunity starts rapidly within 6 h after infection and is inhibited by the virus to varying degrees. The expression of RIG-I and IFN-β decreased on 1–2 days post-infection (dpi). The HPAI H5N8 virus has a stronger inhibitory effect on RIG-I than the low pathogenic avian influenza (LPAI) H4N6 virus and is the strongest in the lungs. After infection with HPAI H5N8 virus, 2 dpi, viral RNA replicates in large amounts in the lungs. It has been proven that RIG-I and IFN-β play an important role in the innate immune response of ducks to HPAI H5N8 virus infection, especially in the lungs. The main battlefield of RIG-I and IFN-β after infection with the LPAI H4N6 virus is in the rectum. Both viruses have been effectively controlled after 7 dpi. These results will help to understand the transmission mechanisms of avian influenza virus in wild ducks and help effectively prevent and control avian influenza.

Highlights

  • Avian influenza, a highly contagious respiratory viral disease caused by the avian influenza virus (AIV), continues to impair the birds and human public health with enormous economic losses alarmingly worldwide

  • Two ducks died in the highly pathogenic avian influenza virus (HPAIV) group, one on the 2nd day and the other on the 5th day, and there was no death in the low pathogenic avian influenza virus (LPAIV) group and the control group

  • The main replication site of HPAIV is in the upper respiratory tract of the host, and it is highly lethal to wild birds (Sturm-Ramirez et al, 2004)

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Summary

Introduction

A highly contagious respiratory viral disease caused by the avian influenza virus (AIV), continues to impair the birds and human public health with enormous economic losses alarmingly worldwide. According to the pathogenicity of AIV to chickens, it is divided into highly pathogenic avian influenza virus (HPAIV) and low pathogenic avian influenza virus (LPAIV). Studies have found that some wild birds (such as whooper swans, cormorants, bar-headed geese, and grebes; Spackman et al, 2009; Okamatsu et al, 2010; Albini et al, 2014; Muzyka et al, 2019) will die on a large scale and quickly after being infected with HPAIV, so they have little effect on the long-distance transmission of the virus. Wild ducks can migrate long distances in an asymptomatic state, and within a certain time frame, the virus can be excreted with their feces to cause influenza transmission

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