Abstract
BackgroundWe examined differences in pathogenicity in pigs from China that had been experimentally infected with porcine reproductive and respiratory syndrome virus (PRRSV).MethodsWe compared pathogenic characteristics of a field isolate (GX-1/2008F), two PRRSV isolates (HN-1/2008, YN-1/2008) propagated in cells, and GX-1/2008F that had been propagated in cells (GX-1/2008). The clinical courses, along with humoral and cell-mediated responses, were monitored for 21 days post-infection (DPI). Animals were sacrificed and tissue samples used for gross pathological, histopathological and ultrastructure examination.ResultsAt 2–3 DPI, animals infected with cell-propagated viruses exhibited signs of coughing, anorexia and fever. However their rectal temperature did not exceed 40.5°C. Viremia was detectable as early as 3 DPI in animals infected with HN-1/2008 and YN-1/2008. Animals inoculated with GX-1/2008F displayed clinical signs at 6 DPI; the rectal temperature of two animals in this group exceeded 41.0°C, with viremia first detected at 7 DPI. Seroconversion for all challenged pigs, except those infected with GX-1/2008, was seen as early as 7 DPI. All of these pigs had fully seroconverted by 11 DPI. All animals challenged with GX-1/2008 remained seronegative until the end of the experiment. Innate immunity was inhibited, with levels of IFN-α and IL-1 not significantly different between control and infected animals. The cytokines IFN-γ and IL-6 transiently increased during acute infection. All virus strains caused gross lesions including multifocal interstitial pneumonia and hyperplasia of lymph nodes. Inflammation of the stomach and small intestine was also observed. Lesions in the group infected with GX-1/2008F were more serious than in other groups. Transmission electron microscopy revealed that alveolar macrophages, plasmacytes and lymphocytes had fractured cytomembranes, and hepatocytes had disrupted organelles and swollen mitochondria.ConclusionsThe pathogenicity of the PRRSV field isolate became attenuated when propagated in MARC-145 cells. Tissue tropism of highly pathogenic strains prevailing in China was altered compared with classical PRRSV strains. The observed damage to immune cells and modulation of cytokine production could be mechanisms that PRRSV employs to evade host immune responses.
Highlights
We examined differences in pathogenicity in pigs from China that had been experimentally infected with porcine reproductive and respiratory syndrome virus (PRRSV)
Differences in pathogenic characteristics between a PRRSV strain from the field (GX-1/2008F), PRRSV strains propagated in cells (HN-1/2008, YN-1/2008) and the field isolate propagated in cells (GX-1/2008) were identified in this comparative study
PRRSV-positive supernatants were passed through 0.22μm filters and adsorbed to MARC-145 cell monolayers grown in Dulbecco’s modified Eagle’s medium (DMEM) containing 2% fetal bovine serum (FBS) for 2 h at 37°C/5% CO2
Summary
We examined differences in pathogenicity in pigs from China that had been experimentally infected with porcine reproductive and respiratory syndrome virus (PRRSV). Porcine reproductive and respiratory syndrome virus (PRRSV) was first identified by Dutch researchers [5] in 1991 as the causative agent of PRRS. Following infection with either genotype, clinical signs are similar and result in respiratory disease and reproductive failure. Infections were characterized by high morbidity (50–100%) with high fever and mortality (20–100%) [10] Since this initial outbreak, the disease has rapidly spread to most of the provinces in China, resulting in more than one million deaths [11]. It would appear that there are as yet unknown differences among strains of PRRSV To investigate these differences we isolated three genotype II PRRSV strains from tissue lesions and compared their pathogenic characteristics. Differences in pathogenic characteristics between a PRRSV strain from the field (GX-1/2008F), PRRSV strains propagated in cells (HN-1/2008, YN-1/2008) and the field isolate propagated in cells (GX-1/2008) were identified in this comparative study
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
