Shrimp autophagy receptor protein PvTAX1BP1 regulates autophagy and facilitates white spot syndrome virus replication in Penaeus vannamei

Abstract

Tax1 binding protein 1 (TAX1BP1) plays a role in autophagy regulation and proteasomal pathway across different species, though its function in shrimp is still being explored. In Penaeus vannamei, the homolog PvTAX1BP1 was characterized by a CALCOCO1 domain, a LC3-interacting region (LIR), two coiled-coil domains, and two ubiquitin-binding zinc finger regions (UBZs). It was ubiquitously expressed in shrimp tissues while its expression in hemocytes was notably downregulated following white spot syndrome virus (WSSV) infection. Silencing PvTAX1BP1 reduced WSSV replication and prolonged shrimp survival, suggesting its involvement in viral pathogenesis. Immunofluorescence assay revealed co-localization of PvTAX1BP1 with the autophagy-related protein PvLC3, indicating a potential interaction and its role in LC3-mediated autophagy. Additionally, knockdown of PvTAX1BP1 resulted in downregulation of the autophagy marker PvLC3-II in WSSV-infected shrimp, reinforcing its role in autophagy regulation during infection. Both yeast two-hybrid (Y2H) and immunofluorescence assays confirmed that PvTAX1BP1 directly interacts with three WSSV proteins: WSSV325, WSSV458, and WSSV517. These findings suggest that PvTAX1BP1 facilitates WSSV replication by modulating host LC3-mediated autophagy, potentially through its interactions with WSSV proteins. This highlights a mechanism by which viruses can exploit cellular processes for their own benefit.