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The colostrum represents an important infection route for many viruses. Here, we demonstrate the vertical transmission of porcine epidemic diarrhea virus (PEDV) from sows to neonatal piglets via colostrum.

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Porcine epidemic diarrhea virus (PEDV) is emerging as a major threat to the global swine industry. Clinical PEDV infection is associated with severe intestinal lesions, resulting in absorptive dysfunction and high mortality rates in suckling piglets. The extracellular matrix (ECM) is an important component of intestinal tissue, providing a structural framework and conveying tissue-specific signals to nearby enterocytes. In this study, we investigated the extensive ECM remodeling observed in intestinal epithelial cells infected with PEDV and elucidated the associated activated ECM receptor-related pathways. Protein-protein interaction network analysis revealed two significantly differentially expressed genes (cluster of differentiation 44 [ CD44 ] and serpin family E member 1 [ SERPINE1 ]) associated with the ECM. At the transcriptional level, both genes exhibited significant positive correlation with the extent of PEDV replication. Similarly, the expression of CD44 and PAI-1 (encoded by SERPINE1 ) was also increased in the intestines of piglets during viral infection. Furthermore, CD44 exhibited antiviral activity by enhancing the expression of antiviral cytokines (e.g., interleukin [IL]-6, IL-18, IL-11, and antimicrobial peptide beta-defensin 1) by activating nuclear factor-κB signaling. Conversely, PAI-1 was found to promote the release of progeny virions during PEDV infection, despite a decreased intracellular viral load. Nevertheless, the underlying mechanisms are still unclear. Taken together, our results highlighted the biological roles of specific ECM-regulated genes, i.e., CD44 and SERPINE1 in suppressing and promoting PEDV infection, thereby providing a theoretical foundation for the role of the ECM in intestinal infections and identifying potential therapeutic targets for PEDV.

Red blood cells (RBCs) are the most abundant cell type in the bloodstream, serving for oxygen transport. Although RBCs have been considered as possible vehicles of virus transmission to target cells, the mechanism is much less well understood. Here, we showed that porcine epidemic diarrhea virus (PEDV), a coronavirus that caused acute and devastating intestinal disease in suckling piglets, could cause typical diarrhea in newborn piglets through hijacking RBCs. Firstly, PEDV could bind and internalize into neonatal RBCs through CD71 and clathrin-mediated endocytosis, and maintain its viability for 12 h. Subsequently, after autotransfusion with PEDV-loaded RBCs, PEDV could infect and colonize intestinal epithelial cells, causing typical diarrhea symptoms in newborn piglets. Moreover, PEDV-loaded RBCs could transfer the virus to CD3+ T cells by formation conjugation structure. PEDV could continue to hitchhike CD3+ T cells to reach intestine mucosa and cause infection. Finally, PEDV-loaded RBCs were found in nasal capillary after intranasal infection with PEDV. Further, higher oxygen concentration was determined as a promoter of PEDV binding RBCs. Therefore, nasal capillary was speculated to be the entry for PEDV binding RBCs. Collectively, our studies illustrated the mechanism that PEDV could cause intestine infection through hijacking RBCs, further providing a novel insight into the role of RBCs in coronavirus pathogenesis as potential cells for viral transmission.