Swine Enteric Coronavirus: Diverse Pathogen–Host Interactions

Abstract

Swine enteric coronavirus (SeCoV) causes acute gastroenteritis and high mortality in newborn piglets. Since the last century, porcine transmissible gastroenteritis virus (TGEV) and porcine epidemic diarrhea virus (PEDV) have swept farms all over the world and caused substantial economic losses. In recent years, porcine delta coronavirus (PDCoV) and swine acute diarrhea syndrome coronavirus (SADS-CoV) have been emerging SeCoVs. Some of them even spread across species, which made the epidemic situation of SeCoV more complex and changeable. Recent studies have begun to reveal the complex SeCoV–host interaction mechanism in detail. This review summarizes the current advances in autophagy, apoptosis, and innate immunity induced by SeCoV infection. These complex interactions may be directly involved in viral replication or the alteration of some signal pathways.

DNAJA3 Interacts with PEDV S1 Protein and Inhibits Virus Replication by Affecting Virus Adsorption to Host Cells

“…Similar to most coronaviruses, PEDV has a coronoid process formed with a trimer spike (S) protein [17]. Its binding with the receptor(s) is the initial event for the virus to invade cells, and it is also adept in using various components of host cells to promote replication and host pathogenesis [38]. Here, we show that DNAJA3, a member of the Hsp40 family, interacts with PEDV S1 and inhibits viral adsorption to the IPEC-J2 cells while PEDV infection could downregulate its expression.…”

“…The S1 protein was selected in this study as bait to screen host proteins in the porcine enteroid cDNA library because of its roles in binding to the host cells [38] and in interacting with the viral accessory protein ORF3, which is involved in PEDV replication [39]. Of the 15 host proteins showing putative binding with S1 from the cDNA library screening, 4 proteins clearly interacted with PEDV S1 through verification with paired yeast…”

“…The hTid-1 isoforms are reported to interact with Jak2 and Hsp70/Hsc70 and modulate IFN-γ-mediated transcriptional activity, and the interaction between Hsp70/Hsc70 and hTid-1 is reduced after IFN-γ treatment [50]. Recent studies have indicated that such cellular events and signaling are involved during PEDV infection [38,51,52]. Further research is required to determine if and how DNAJA3 functions in regulating PDEV replication inside the cells.…”

“…The life cycle of PEDV includes adsorption, endocytosis, replication, and virion release [38]. To examine if DNAJA3 affects PEDV infection at the adsorption or internalization stage, we pre-treated the IPEC-J2 cells with DNAJA3 silencing or overexpressing vectors which were then infected with a high infection dose of PEDV (MOI = 5) for adsorption at 4 • C for 1 h or shifted to 37 • C for 1 h to estimate virus entry.…”

Historical Evolutionary Dynamics and Phylogeography Analysis of Transmissible Gastroenteritis Virus and Porcine Deltacoronavirus: Findings from 59 Suspected Swine Viral Samples from China

“…Swine enteric coronaviruses (SeCoVs) are coronaviruses with swine intestinal tissue tropism, causing watery diarrhea, vomiting, and even death in sows and piglets [ 9 ]. At present, four SeCoVs have been identified, namely transmissible gastroenteritis virus (TGEV), porcine epidemic diarrhea virus (PEDV), porcine deltacoronavirus (PDCoV), and severe acute diarrhea syndrome coronavirus (SADS-CoV).…”