The cytoplasmic tail of IBV spike mediates intracellular retention via interaction with COPI-coated vesicles in retrograde trafficking

• DOI: 10.1128/jvi.02164-24
• Publication Date: 2025-01-22T14:00:27Z
• Authors: Rong Liang; Jiaxin Tian; Kangchengyin Liu; Liman Ma; Ruihua Yang; Lu Sun; Jing Zhao; Ye Zhao; Guozhong Zhang
• Keywords: COPI; COPII; Transport protein

ABSTRACT Coronaviruses are characterized by their progeny assembly and budding in the endoplasmic reticulum-Golgi intermediate compartment (ERGIC). Our previous studies demonstrated that truncation of 9 amino acids cytoplasmic tail (CT) infectious bronchitis virus (IBV) spike (S) protein impairs its localization to ERGIC, resulting increased expression at plasma membrane. However, precise mechanism underlying this phenomenon remained elusive. In study, we provide evidence IBV S could utilize coatomer protein-I (COPI)-coated vesicles for retrograde transport from Golgi reticulum (ER). We identified KKSV motif as critical binding site within CT domain COPI interaction. Further analysis reveals infection does not modulate host expression. when is disrupted, a higher proportion escapes Moreover, inhibition COPI-mediated during viral severely virion production leads accumulation membrane, inducing cell-cell fusion syncytia formation. findings contribute deeper understanding intracellular trafficking coronavirus infection, offer valuable insights into molecular mechanisms replication cell biology. IMPORTANCE Viruses hijack or modify cellular machiner y associated pathways facilitate own replication. Here, demonstrate directly interacts with through tail. COPI-coated mediate apparatus compartment, where particle occurs. only advance our but also developing more effective vaccine strategies.