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Porcine reproductive and respiratory syndrome (PRRS) is a highly contagious and pathogenic infectious disease caused by the porcine reproductive and respiratory syndrome virus (PRRSV). It manifests as reproductive disorders in sows and respiratory disorders in piglets. PRRSV infects swine herds with symptoms such as abortions, stillbirths, and mummified fetuses in gestating sows. Piglets mainly experience abdominal respiration and respiratory symptoms. To date, the prevention of PRRS relies primarily on vaccination and the implementation of various preventive and control measures. Swine deaths caused by PRRS have resulted in significant economic losses to the pig industry worldwide. Non-structural protein 10 (NSP10) has helicase and adenosine triphosphatase (ATPase) activities that unwind DNA and RNA and play important roles in viral replication and transcription. Hence, it can be potentially used to develop novel reagents for the detection of PPRSV. This article reviews genetic variations, interaction with viral and host proteins, effects on PRRSV replication, immunomodulation, apoptosis, and viral virulence of NSP10, with the aim of providing a theoretical basis for the prevention and control of PRRS and drug development in the future. [ABSTRACT FROM AUTHOR]

Porcine reproductive and respiratory syndrome (PRRS) is considered to be one of the most important infectious diseases impacting the swine industry and is characterized by reproductive failure in late term gestation in sows and respiratory disease in pigs of all ages. The nonstructural protein 9 gene, Nsp9, encoding the RNA-dependent RNA polymerase, is generally regarded as fairly conserved when compared to other viral proteins. Antibodies against Nsp9 will be of great importance for the diagnosis and treatment of the causal agent, PRRS virus. A study was undertaken to generate polyclonal antibodies against the immunodominant Nsp9. For this purpose, the Nsp9 was expressed in Escherichia coli and subsequently used as an antigen to immunize New Zealand rabbits. Antiserum was identified via an indirect ELISA, and then verified based on the ability to react with both naturally and artificially expressed Nsp9. Results of virus neutralization test showed that this antiserum could not neutralize the PRRSV. Nevertheless, this antiserum as a diagnostic core reagent should prove invaluable for further investigations into the mechanism of PRRS pathogenesis.

Abstract Porcine reproductive and respiratory syndrome virus (PRRSV) has previously been shown to increase porcine 2′-5′-oligoadenylate synthase (OAS) 1a expression, but the specific role of porcine OAS1b (pOAS1b) in PRRSV replication remains unknown. In this study, we conducted sequence analysis of the porcine OAS1b gene and studied the effects of its overexpression or silencing on PRRSV replication. OAS1b, localized mainly in the cytoplasm, was found to contain conserved protein domains, such as the P-Loop and D-Box, indicating that its nucleotidyl transferase activity was complete and the antiviral effect depended on ribonuclease L (RNase L). OAS1b overexpression inhibited PRRSV replication, whereas small-interfering-RNA silencing of OAS1b resulted in increased virus titers. Additionally, OAS1b promoted expression of interferons as well as interferon-β promoter activity. These results lay the theoretical foundation for the development of new anti-PRRSV strategies. [ABSTRACT FROM AUTHOR]

Stimulator of interferon gene (STING), an adaptor molecule in the immune system, is involved in mediating the response to viral and bacterial infections, anti-tumor immunity, autoimmune diseases, and lipid metabolism. There have been reports on the cloning and function of STING in humans, pigs, chickens, and cats; however, STING has not been characterized in non-human primates or monkeys to date. Therefore, in this study, the rhesus macaque (Macaca mulata) STING gene was cloned, and we performed preliminary functional tests to examine its role in the interferon (IFN) pathway. The M. mulatta STING complementary DNA was 1140 bp in length and encoded 380 amino acid residues. Phylogenetic analysis showed that Homo sapiens and M. mulatta STING are closely related and clustered on the same branch. M. mulatta STING was confirmed to increase the promoter activities of IFN-β, nuclear factor-κB, and interferon-sensitive response element, and STING overexpression increased the mRNA levels of IFN-α, IFN-β, and interferon regulatory factor 3. Infection of Marc-145 cells with porcine reproductive and respiratory syndrome virus activated STING, and its expression increased along with increases in viral multiplicity of infection titer and time. Moreover, STING expression was time- and dose-dependently up-regulated by poly (I:C) and poly (dA:dT) treatments in Marc-145 cells. In summary, these results highlight STING as a vital immune system signal protein in the IFN pathway. This study provides a basis for understanding the immune characteristics of M. mulatta , and may have important implications for both monkey and human diseases. • Macaca mulatta stimulator of interferon gene (STING) was cloned for the first time. • Human and M. mulatta STING show high sequence similarity and cluster on the same branch. • M. mulatta STING actives the interferon pathway. • PRRSV, poly(I:C), and poly(dA:dT) increase the STING expression level in monkey cells. [ABSTRACT FROM AUTHOR]