Porcine epidemic diarrhea (PED) is a contagious intestinal disease caused by Porcine epidemic diarrhea virus (PEDV) that characterized by vomiting, diarrhea, and dehydration. PEDV was first identified in the 1980s in China, and since then, it has become one of the most common viral causes of diarrhea. In October 2010, a large-scale outbreak of PED caused by a PEDV variant occurred in China, resulting in tremendous economic losses. This review presents a comprehensive description of PEDV history, prevalence, molecular features, and prevention and control strategies in China.

Porcine epidemic diarrhea virus (PEDV),

No abstract

The research of carbon-based antivirals is still in its infancy, and their development into safe and effective carbon dots (CDs) with antiviral activity at multiple points in the life cycle of the virus remains to be explored. Here, we report a one-step method to apply curcumin in order to prepare of uniform and stable cationic carbon dots (CCM-CDs) with antiviral properties. The inhibitory effect of CCM-CDs on viral replication was studied by using porcine epidemic diarrhea virus (PEDV) as a coronavirus model. PEDV is applied as a coronavirus model to study the antiviral effect of as-prepared CCM-CDs on its replication. The cationic CCM-CDs treatment is found obviously to inhibit the proliferation of PEDV compared with the common CDs (EDA-CDs). The CCM-CDs treatment can change the structure of surface protein in viruses, thereby inhibiting viral entry. It can also suppresses the synthesis of negative-strand RNA of the virus, the budding of the virus, and the accumulation of reactive oxygen species by PEDV. Furthermore, CCM-CDs treatment is also found to suppress viral replication by stimulating the production of interferon-stimulating genes (ISGs) and proinflammatory cytokines. These results offer theoretical support for the development of CCM-CDs as a hopeful antiviral drug for the treatment of coronavirus infections, including PEDV.

Porcine epidemic diarrhea virus (PEDV) is

Development of novel antiviral reagents is of great importance for the control of virus spread. Here, AgS nanoclusters (NCs) were proved for the first time to possess highly efficient antiviral activity by using porcine epidemic diarrhea virus (PEDV) as a model of coronavirus. Analyses of virus titers showed that AgS NCs significantly suppressed the infection of PEDV by about 3 orders of magnitude at the noncytotoxic concentration at 12 h postinfection, which was further confirmed by the expression of viral proteins. Mechanism investigations indicated that AgS NCs treatment inhibits the synthesis of viral negative-strand RNA and viral budding. AgS NCs treatment was also found to positively regulate the generation of IFN-stimulating genes (ISGs) and the expression of proinflammation cytokines, which might prevent PEDV infection. This study suggest the novel underlying of AgS NCs as a promising therapeutic drug for coronavirus.

Foot-and-mouth disease is a highly contagious viral illness of wild and domestic cloven-hoofed animals. The causative agent, foot-and-mouth disease virus (FMDV), replicates rapidly, efficiently disseminating within the infected host and being passed on to susceptible animals via direct contact or the aerosol route. To survive in the host, FMDV has evolved to block the host interferon (IFN) response. Previously, we and others demonstrated that the leader proteinase (L pro ) of FMDV is an IFN antagonist. Here, we report that another FMDV-encoded proteinase, 3C pro , also inhibits IFN-α/β response and the expression of IFN-stimulated genes. Acting in a proteasome- and caspase-independent manner, the 3C pro of FMDV proteolytically cleaved nuclear transcription factor kappa B (NF-κB) essential modulator (NEMO), a bridging adaptor protein essential for activating both NF-κB and interferon-regulatory factor signaling pathways. 3C pro specifically targeted NEMO at the Gln 383 residue, cleaving off the C-terminal zinc finger domain from the protein. This cleavage impaired the ability of NEMO to activate downstream IFN production and to act as a signaling adaptor of the RIG-I/MDA5 pathway. Mutations specifically disrupting the cysteine protease activity of 3C pro abrogated NEMO cleavage and the inhibition of IFN induction. Collectively, our data identify NEMO as a substrate for FMDV 3C pro and reveal a novel mechanism evolved by a picornavirus to counteract innate immune signaling.

No abstract