<p>Porcine epidemic diarrhea virus (PEDV) has caused significant losses in the pork industry, but the mechanism of PEDV infection is still unclear. On the basis of our RNA-Seq data and due to the potential role of sialic acid as a coreceptor, we investigated the function of sialic acid-binding Ig-like lectin 15 (Siglec-15) to determine its role as a receptor in PEDV infection. We found that Siglec-15 enhances PEDV infection by promoting viral adsorption to host cells. Coimmunoprecipitation and immunofluorescence assays revealed that Siglec-15 binds to the S1 subunit and M protein of PEDV. PEDV infectivity was significantly reduced in Siglec-15 knockout mice. In addition, we developed a monoclonal antibody targeting Siglec-15 that can effectively inhibit PEDV infection both in vitro and in vivo. Overall, our study suggests that Siglec-15 may be a receptor for PEDV infection, which is important for related mechanistic studies and reveals a novel target for anti-PEDV therapeutic development.</p>

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Siglec-15 is a putative receptor for porcine epidemic diarrhea virus infection

  • Zhihua Feng,
  • Yajuan Fu,
  • Sheng Yang,
  • Heng Zhao,
  • Minhua Lin,
  • Chuancheng Liu,
  • Weili Huang,
  • Xinyan He,
  • Yao Chen,
  • Jianxin Chen,
  • Yangkun Shen,
  • Zhaolong Li,
  • Qi Chen

摘要

Porcine epidemic diarrhea virus (PEDV) has caused significant losses in the pork industry, but the mechanism of PEDV infection is still unclear. On the basis of our RNA-Seq data and due to the potential role of sialic acid as a coreceptor, we investigated the function of sialic acid-binding Ig-like lectin 15 (Siglec-15) to determine its role as a receptor in PEDV infection. We found that Siglec-15 enhances PEDV infection by promoting viral adsorption to host cells. Coimmunoprecipitation and immunofluorescence assays revealed that Siglec-15 binds to the S1 subunit and M protein of PEDV. PEDV infectivity was significantly reduced in Siglec-15 knockout mice. In addition, we developed a monoclonal antibody targeting Siglec-15 that can effectively inhibit PEDV infection both in vitro and in vivo. Overall, our study suggests that Siglec-15 may be a receptor for PEDV infection, which is important for related mechanistic studies and reveals a novel target for anti-PEDV therapeutic development.