Differential response of porcine immature monocyte-derived dendritic cells to virulent and inactivated transmissible gastroenteritis virus

Abstract

Exposure of piglets less than 2 weeks of age to virulent transmissible gastroenteritis virus (TGEV) gives rise to mortality as high as 100%, and adult pigs recovering from its infection often become TGEV carriers. These facts suggest an evasion of the immune system by virulent TGEV. In this study, we showed that a virulent TGEV SHXB strain could infect porcine immature monocyte-derived dendritic cells (Mo-DCs), and down-regulate cell surface markers (SLA-II-DR, CD1a and CD80/86). Moreover, SHXB-infected immature Mo-DCs showed low expression of IL-12 and IFN-γ, and also lost the ability to stimulate T cell proliferation. Finally, SHXB inhibited the activation of nuclear factor kappa B (NF-κB) in these cells. Instead, UV-inactivated SHXB (UV-SHXB) had the opposite effects in immature Mo-DCs. In conclusion, the virulent SHXB could severely impair immature Mo-DCs, which might be involved in the pathogenesis of virulent TGEV in vivo.

TGEV non-structural protein ORF3b up-regulates the expression of SLA-DR at transcriptional level in monocyte-derived porcine dendritic cells

“…Porcine Epidemic Diarrhea Virus (PEDV) infection with immature DCs stimulated the production of IL-12 and IFNγ [17]. TGEV can infect both immature and mature DCs, while the expression of IL-12 in infected immature DCs is lower, and does not stimulate T cell proliferation [13].…”

“…It is critical to understand the mechanisms of dendritic cell impacting a variety of immune system processes, including antigen processing and presentation [12]. A previous study con rmed that TGEV has the ability to infect DCs [13].…”

Transmissible Gastroenteritis Virus: An Update Review and Perspective

“…However, it has been reported that not all strains carrying this 6nt deletion are all attenuated strains. For example, the SHXB strain isolated in China is considered to be a lethal virulent strain after being verified by an animal challenge test [ 103 , 104 ]. The specific reason for the phenomenon of strains carrying the deletion sites that were previously considered to be classical attenuated strains but still being virulent strains is not clear, which may be caused by mutations in other undiscovered sites in the viral genome.…”

“…Therefore, the mutation of amino acid 585 from serine to alanine may be one of the reasons for the reduced virulence of TGEV strains [ 68 ]. However, some strains that also carry this mutation have been shown to be virulent, such as the AHHF and SHXB strains [ 6 , 103 ]. The reason for this phenomenon contradicting the previous conclusion is not clear, so whether the S585A locus can indeed lead to the attenuation of TGEV virulence needs to be proved by reverse genetics.…”

H9N2 avian influenza virus enhances the immune responses of BMDCs by down-regulating miR29c

“…After another 24 h, BMDCs were collected and total RNA was extracted with trizol reagents.RT-PCR was then performed according to instructions (TaKaRa). Virus PB1 and NP gene was choose as the target gene and the mouse GAPDH gene was used as the internal parameter (primers were list in Supplementary table 3)[24,25]. Quantification of the target gene was determined by relative standard curves.…”