Porcine reproductive and respiratory syndrome virus (PRRSV) could be sensed by professional beta interferon-producing system and had mechanisms to inhibit this action in MARC-145 cells

Abstract

Porcine reproductive and respiratory syndrome virus (PRRSV) causes an economically important disease in swine-producing area, and interferon beta (IFN-beta) is the first responder against the animal virus infection. However, whether PRRSV could induce the production of IFN-beta is controversial. In this paper, we first time found that PRRSV could phosphorylate IFN-regulatory factor 3 (IRF-3) and weakly activate the IFN-beta promoter in MARC-145 cells in early infection, but the activations of IRF-3 and IFN-beta promoter were rapidly inhibited in the following infection. Furthermore, which components or products of the invading PRRSV cause PRRSV to inhibit IFN-beta promoter activity attracted our attentions. The obtained results showed that PRRSV nsp1 could inhibit Poly(I:C)-induced IFN-beta promoter activity in MARC-145 cells by down-regulating the protein level of IRF-3 and inhibiting the phosphorylation of IRF-3. In conclusion, our results suggested that PRRSV could be sensed by professional IFN-beta-producing system and had mechanisms to inhibit this action in MARC-145 cells.

Endoribonuclease activities of porcine reproductive and respiratory syndrome virus nsp11 was essential for nsp11 to inhibit IFN-β induction

“…Our previous study found that PRRSV could weakly trigger the activation of IRF-3 as well as induce the activation of IFN-␤ promoter at 24 h p.i., but their activities were rapidly inhibited in following infection. That is, PRRSV could be sensed by professional beta interferon-producing system in MARC-145 cells and had mechanisms to inhibit this action in MARC-145 cells (Shi et al, 2010). So our present work supplied another evidence that the endoribonuclease of PRRSV nsp11 could antagonize the induction of IFN-␤.…”

“…Our previous study and others have found that nsp1, nsp2 and nsp11 from PRRSV were the IFN antagonists (Beura et al, 2010;Shi et al, 2010). Sun et al (2010) found that ubiquitindeconjugating activity of nsp2 antagonized the type I interferon.…”

“…ORF1a and ORF1b could produce 14 nonstructural proteins (nsp1␣, nsp1␤, nsp2, nsp3, nsp4, nsp5, nsp6, nsp7␣, nsp7␤, nsp8, nsp9, nsp10, nsp11 and nap12) (den Boon et al, 1991;Fang and Snijder, 2010). Our previous study and others have found that PRRSV suppressed IFN-␤ production induced by Poly(I:C) (Luo et al, 2008) and that nsp1, nsp2 and nsp11 from PRRSV were the IFN antagonists (Beura et al, 2010;Shi et al, 2010). Sun et al (2010) found that ubiquitin-deconjugating activity of nsp2 antagonized the type I interferon.…”

“…The p-284 Luc (positions −284 and +19 in IFN-␤ gene prior to the luciferase report gene) and phRL-TK plasmids have already been described (Shi et al, 2010). pcDNA3.1-FLAG was constructed by using FLAG primers (Forward: CTAGCTAGCGCCACCATGGAT-TACAAGGATGACGA and Reverse: TCAGAAGCTTGCCTTATCGTCGT-CATCCTTGTAATCCA).…”

Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Modulates Interferon-β Expression Mainly Through Attenuating Interferon-Regulatory Factor 3 Phosphorylation

“…P orcine reproductive and respiratory syndrome (PRRS) is an emergent catastrophic swine disease characterized by serious reproductive failure in pregnant sows and severe respiratory distress in piglets and growing pigs (Suradhat and Thanawongnuwech, 2003;Diaz et al, 2005;Shi et al, 2010). The culprit in PRRS is a positivestranded RNA virus of the order Nidovirales and family Arteriviridae called PRRS virus (PRRSV) (Ropp et al, 2004), which delays neutralizing antibody response and causes viremia and persistent infection leading to PRRS (Plagemann, 2004).…”