Key Laboratory of Animal Epidemiology and Zoonosis of Ministry of Agriculture, College of Veterinary Medicine and State Key Laboratory of Agribiotechnology, China Agricultural University, Beijing, People's Republic of China.
Published: August 2012
AI Article Synopsis
Article Abstract
In this study, we confirmed the autophagy induced by porcine reproductive and respiratory syndrome virus (PRRSV) in permissive cells and investigated the role of autophagy in the replication of PRRSV. We first demonstrated that PRRSV infection significantly results in the increased double-membrane vesicles, the accumulation of LC3 fluorescence puncta, and the raised ratio of LC3-II/β-actin, in MARC-145 cells. Then we discovered that induction of autophagy by rapamycin significantly enhances the viral titers of PRRSV, while inhibition of autophagy by 3-MA and silencing of LC3 gene by siRNA reduces the yield of PRRSV. The results showed functional autolysosomes can be formed after PRRSV infection and the autophagosome-lysosome-fusion inhibitor decreases the virus titers. We also examined the induction of autophagy by PRRSV infection in pulmonary alveolar macrophages. These findings indicate that autophagy induced by PRRSV infection plays a role in sustaining the replication of PRRSV in host cells.
We investigated whether environmental enrichment applied at different life stages of pigs affects the susceptibility to and severity of disease by studying immune cell functions around weaning and during nursery, the effects of infection in models and using a co-infection model of (PRRSV) followed by an infection. Pigs were either conventionally housed (CCH) or enriched housed throughout life, with enrichment consisting of extra space, rooting materials and co-mingling with another litter before weaning (EEH), or they were switched from conventional to enriched housing at weaning (CEH). Sixty days after birth, ten pigs per treatment were infected with PRRSV followed by an infection eight days later.
Unlabelled: Recombination is a significant factor driving the evolution of RNA viruses. The prevalence and variation of porcine reproductive and respiratory syndrome virus (PRRSV) in China have been increasing in complexity due to extensive interlineage recombination. When this recombination phenomenon occurs in live vaccine strains, it becomes increasingly difficult to prevent and control PRRSV.
Porcine Reproductive and Respiratory Syndrome (PRRS) causes huge economic losses to pig farms worldwide. Currently available vaccines do not always offer complete protection, due to the extreme variability of the virus. Therefore, good farming practices must be improved to prevent the disease from spreading across the pig production system.
Breeding animals to produce more robust and disease-resistant pig populations becomes a complementary strategy to the more conventional methods of biosecurity and vaccination. The objective of this study was to explore the ability of a panel of genetic markers and immunity parameters to predict the survival rates during a natural PRRSV outbreak. Ten-week-old female Duroc pigs (n = 129), obtained from 61 sows and 20 boars, were naturally infected with a highly pathogenic PRRSV genotype 1 strain.
N-methyladenosine (mA) is a prevalent and dynamic RNA modification, critical in regulating gene expression. Recent research has shed light on its significance in the life cycle of viruses, especially animal viruses. Depending on the context, these modifications can either enhance or inhibit the replication of viruses.
