scholarly journals Age-dependent variation in innate immune responses to porcine epidemic diarrhea virus infection in suckling versus weaned pigs

2015 ◽  
Vol 168 (3-4) ◽  
pp. 193-202 ◽  
Author(s):  
Thavamathi Annamalai ◽  
Linda J. Saif ◽  
Zhongyan Lu ◽  
Kwonil Jung
Keyword(s):  
Virus Infection ◽  
Immune Responses ◽  
Porcine Epidemic Diarrhea Virus ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Weaned Pigs ◽  
Diarrhea Virus ◽  
Age Dependent ◽  
Porcine Epidemic Diarrhea

scholarly journals Porcine epidemic diarrhea virus inhibits HDAC1 expression to facilitate its replication via binding of its nucleocapsid protein to host transcription factor Sp1

2021 ◽  
Author(s):  
Jidong Xu ◽  
Junyong Mao ◽  
Xiao Han ◽  
Fushan Shi ◽  
Qin Gao ◽  
...  
Keyword(s):  
Immune Responses ◽  
Histone Deacetylases ◽  
Porcine Epidemic Diarrhea Virus ◽  
Innate Immune ◽  
Host Responses ◽  
Innate Immune Responses ◽  
N Protein ◽  
Diarrhea Virus ◽  
Neonatal Pigs ◽  
Porcine Epidemic Diarrhea

Porcine epidemic diarrhea virus (PEDV) is an enteric coronavirus causing acute intestinal infection in pigs, with high mortality often seen in neonatal pigs. The newborns rely on innate immune responses against invading pathogens because of lacking adaptive immunity. However, how PEDV disables the innate immunity of newborns towards severe infection remains unknown. We found that PEDV infection led to reduced expression of histone deacetylases (HDACs), especially HDAC1 in porcine IPEC-J2 cells. HDACs are considered as important regulators of innate immunity. We hypothesized that PEDV might interact with certain host factors to regulate HDAC1 expression in favor of its replication. We show that HDAC1 acted as a negative regulator of PEDV replication in IPEC-J2 cells, as shown by chemical inhibition, gene knockout and overexpression. A GC-box ( GCCCCACCCCC ) within the HDAC1 promoter region was identified for Sp1 binding in IPEC-J2 cells. Treatment of the cells with Sp1 inhibitor, mithramycin A, inhibited HDAC1 expression, indicating direct regulation of HDAC1 expression by Sp1. Of the viral proteins that were overexpressed in IPEC-J2 cells, the N protein was found to be present in the nuclei and more inhibitory to HDAC1 transcription. The putative NLS 261 PKKNKSR 267 contributed to its nuclear localization. The N protein interacted with Sp1 and interfered with its binding to the promoter region, thereby inhibiting its transcriptional activity for HDAC1 expression. Our findings reveal a novel mechanism of PEDV evasion of the host responses, offering implications for studying the infection processes of other coronaviruses. Importance The enteric coronavirus porcine epidemic diarrhea virus (PEDV) causes fatal acute intestinal infection in neonatal pigs that rely on innate immune responses. Histone deacetylases (HDACs) play important roles in innate immune regulation. Our study found PEDV suppresses HDAC1 expression via the interaction of its N protein and porcine Sp1, which identified a novel mechanism of PEDV evasion of the host responses to benefit its replication. This study suggests that other coronaviruses, including SARS-CoV and SARS-CoV-2, may also make use of their N proteins to intercept the host immune responses in favor of their infection.

scholarly journals Immunogenicity of Recombinant-Deficient Lactobacillus casei with Complementary Plasmid Expressing Alanine Racemase Gene and Core Neutralizing Epitope Antigen against Porcine Epidemic Diarrhea Virus

Vaccines ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 1084
Author(s):  
Fengsai Li ◽  
Xiaona Wang ◽  
Xiaolong Fan ◽  
Ling Sui ◽  
Hailin Zhang ◽  
...  
Keyword(s):  
Immune Responses ◽  
Porcine Epidemic Diarrhea Virus ◽  
Lactobacillus Casei ◽  
Oral Vaccine ◽  
Mucosal Vaccine ◽  
Alanine Racemase ◽  
Main Function ◽  
Neutralizing Epitope ◽  
Diarrhea Virus ◽  
Porcine Epidemic Diarrhea

Porcine epidemic diarrhea (PED), which is caused by the porcine epidemic diarrhea virus (PEDV), has occurred worldwide and poses a serious threat to the pig industry. Intestine is the main function site of PEDV; therefore, it is important to develop an oral mucosal immunity vaccine against this virus infection. Most traditional plasmid delivery vectors use antibiotic genes as a selective marker, easily leading to antibiotic accumulation and gene contamination. In this study, to explore whether the alanine racemase gene (Alr) could be used as a screening marker and develop an efficient oral vaccine against PEDV infection, a recombinant strain was constructed using Lactobacillus casei with Alr deletion (L. casei ΔAlr W56) to deliver the Alr gene and a core-neutralizing epitope (COE) antigen. This recombinant bacterium efficiently induced secretory immunoglobulin A (SIgA)-based mucosal and immunoglobulin G (IgG)-based humoral immune responses via oral vaccination in mice. Compared to the other strains, the recombinant bacteria were able to grow without the addition of D-alanine, revealing that Alr in the plasmid could function normally in defective bacteria. This oral mucosal vaccine would provide a useful strategy to substitute the application of antibiotics in the future and induce efficient immune responses against PEDV infection.

scholarly journals Dietary 25-Hydroxyvitamin D3 Supplementation Alleviates Porcine Epidemic Diarrhea Virus Infection by Improving Intestinal Structure and Immune Response in Weaned Pigs

Animals ◽  
2019 ◽  
Vol 9 (9) ◽  
pp. 627 ◽  
Author(s):  
Jiwen Yang ◽  
Gang Tian ◽  
Daiwen Chen ◽  
Ping Zheng ◽  
Jie Yu ◽  
...  
Keyword(s):  
Immune Response ◽  
Porcine Epidemic Diarrhea Virus ◽  
Average Daily Gain ◽  
Intestinal Damage ◽  
Weaned Pigs ◽  
Diarrhea Virus ◽  
Crypt Depth ◽  
Inflammatory Status ◽  
Villous Height ◽  
Porcine Epidemic Diarrhea

We conducted this experiment to determine if feeding 25-hydroxyvitamin D3 (25(OH)D3) to weaned pigs would alleviate porcine epidemic diarrhea virus (PEDV) infection and immune response. Forty-two weaned pigs were allotted to 1 of 6 dietary 25(OH)D3 treatments (5.5, 5.5, 43.0, 80.5, 118.0, 155.5 μg 25(OH)D3/kg diet) for 26 days. On day 22 of the trial, all the treatments were orally administrated with PEDV except for one of the 5.5 μg 25(OH)D3/kg treatments, which was challenged with the same volume of sterile saline and served as control. Another 5.5 μg 25(OH)D3/kg group for PEDV challenge was named CON-PEDV. Average daily gain (p < 0.05) was reduced by PEDV infection. PEDV administration also induced severe diarrhea (p < 0.05), reduction of villous height and the ratio of villous height to crypt depth, and increase of crypt depth and serum diamine oxidase activity (p < 0.05). Serum IgM and complement component 4 levels were increased by PEDV challenge. However, 155.5 μg 25(OH)D3/kg supplementation alleviated intestinal damage (p < 0.05) compared with CON-PEDV. Furthermore, 155.5 μg 25(OH)D3/kg supplementation downregulated the mRNA abundance of inflammatory cytokines and interferon signal pathway-related genes (p < 0.05) compared with CON-PEDV. These results suggested that dietary supplementation of 155.5 μg 25(OH)D3/kg could alleviate intestinal damage and protect against PEDV-induced inflammatory status.

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