Interplay between CTHRC1 and the SU protein of avian leukosis virus subgroup J (ALV-J) facilitates viral replication

• DOI: 10.1016/j.virusres.2019.02.014
• Publication Date: 2019-02-22T02:29:03Z
• Authors: Yu Pang; Defang Zhou; Jingwen Xue; Jing Zhou; Ya Zhang; Gaoying Zheng; Shiyu Yuan; Yongxiu Yao; Ziqiang Cheng
• Keywords: Proteomics; Extracellular Matrix Proteins; 0303 health sciences; Avian Leukosis Virus; Host Microbial Interactions; Chick Embryo; Fibroblasts; Virus Replication; Cell Line; 3. Good health; 03 medical and health sciences; Viral Envelope Proteins; Animals; Chickens

The lifecycle of avian leukosis virus subgroup J (ALV-J), a typical tumorigenic retrovirus, is highly dependent upon host cellular proteins. However, there have been few studies directed at uncovering the host proteins responsible for ALV-J replication, which could provide insights into new strategies for ALV-J prevention and control. Here, we used proteomics to identify the association of differential levels of collagen triple helix-repeat-containing 1 (CTHRC1) and with viral replication. Our results revealed that CTHRC1 was significantly upregulated in ALV-J-infected cells in vitro, and these findings were confirmed in vivo. Additionally, CTHRC1 overexpression facilitated ALV-J replication, whereas CTHRC1 knockdown suppressed this activity. Moreover, we found that ALV-J drove CTHRC1 translocation from the nucleus to the cytosol through interactions with the ALV-J envelope glycoprotein. These results revealed CTHRC1 as a shutting protein is recruited by ALV-J to facilitate viral replication.