Porcine sialoadhesin suppresses type I interferon production to support porcine reproductive and respiratory syndrome virus infection

Yingqi Liu,Songlin Qiao,Xin-Xin Chen,Rui Li,Gaiping Zhang,Ruiguang Deng

doi:10.1186/s13567-020-00743-7

Abstract

Porcine reproductive and respiratory syndrome virus (PRRSV) is a significant threat to the global swine industry. Porcine sialoadhesin (poSn) has been previously shown to mediate PRRSV attachment and internalization. In the current study, we report its unidentified role in antagonism of type I interferon (IFN) production during PRRSV infection. We determined that poSn facilitated PRRSV infection via inhibition of type I IFN transcription. Mechanistically, poSn interacted with a 12 kDa DNAX-activation protein (DAP12), which was dependent on residues 51–57 within DAP12 transmembrane domain (TMD). PRRSV exploited the poSn-DAP12 pathway to attenuate activation of nuclear factor-kappa B (NF-κB). More importantly, the poSn-DAP12 pathway was involved in inhibiting poly (I:C)-triggered IFN production. All these results reveal a novel role of poSn in suppressing host antiviral responses, which deepens our understanding of PRRSV pathogenesis.

Highlights

Porcine reproductive and respiratory syndrome (PRRS) has been causing significant economic losses to the global swine industry [1]
Results Porcine sialoadhesin (poSn) facilitates PRRS virus (PRRSV) infection and inhibits PRRSV‐induced IFN‐α/β transcription To verify the biological significance of poSn during PRRSV infection, we examined the effects of poSn knockdown on PRRSV infection and PRRSV-triggered type I IFN production
We checked PRRSV-induced transcription of type I IFN after poSn knockdown. poSn knockdown promoted the IFN-β transcription (Figure 1D), which suppressed PRRSV infection (Figures 1B and C). All these results suggest that poSn facilitates PRRSV infection by inhibiting the virus-triggered type I IFN production

Summary

Introduction

Porcine reproductive and respiratory syndrome (PRRS) has been causing significant economic losses to the global swine industry [1]. PRRS virus (PRRSV), as the causative agent, belongs to the Porarterivirus genus, Arteriviridae family in the order Nidovirales [3]. It is a single-stranded positive RNA virus with a genome of 14.9 to 15.5 kb in length. Increasing evidence has shown that Siglecs modulate type I interferon (IFN) responses during viral infections. Siglec-G is reported to be induced and exploited by RNA viruses to inhibit retinoic acid-inducible gene-I (RIG-I)-mediated type I IFN production [13]. Siglec-H is demonstrated to negatively regulate IFN-α production in response to murine cytomegalovirus infection in vitro

Methods

Results

Conclusion