data

Previous research has demonstrated that porcine alveolar macrophages (PAMs) express type I complement receptor molecules (CR1-like). Inhibition of CR1-like activity has been shown to reduce the susceptibility of PAMs to porcine reproductive and respiratory syndrome virus (PRRSV) infection, indicating that CR1-like facilitates PRRSV infection; however, the underlying molecular mechanism remains unclear. This study employed techniques such as immunofluorescence, immunoblotting, scanning electron microscopy, immune blocking, and real-time fluorescence quantification to investigate the molecular mechanism underlying CR1-like mediated PRRSV antibody-dependent enhancement. The findings revealed that the binding of CR1-like to the PRRSV antigen-antibody complex induces dynamic alterations in membrane skeleton proteins, thereby facilitating PRRSV entry into PAMs.