Studies of porcine reproductive and respiratory syndrome (PRRS) virus infection in avian species

Late in 1991, an enveloped RNA virus (now called porcine reproductive and respiratory syndrome [PRRS] virus) was identified as the etiologic agent for mystery swine disease. In 1992, laboratory procedures for the diagnosis of this disease evolved rapidly, and veterinary diagnosticians started applying these tests to field cases. This report is written from the perspective of veterinary laboratory diagnosticians and utilizes 3 case studies to define the advantages and disadvantages of the various available diagnostic laboratory PRRS test procedures in different clinical situations. The diagnostic procedures currently used in our laboratory for investigating PRRS are pathologic examination, serologic testing, fluorescent antibody (FA) testing, and virus isolation. Interstitial pneumonia, characterized by mononuclear cell infiltration of alveolar walls with normal airway epithelium, is a hallmark lesion for the disease, especially in neonatal pigs with respiratory distress. Interstitial pneumonia is not a specific lesion and must be coupled with other tests to verify PRRS virus infection. Demonstration of seroconversion is helpful, especially in sows that have experienced reproductive failure. The indirect FA test detects antibody sooner than the serum neutralization test and will likely become the serologic test of choice. The direct FA test on fresh tissue utilizes monoclonal antibody and is useful for investigating PRRS virus-associated pneumonia. Virus isolation utilizing swine alveolar macrophages has also been a useful diagnostic procedure. All of the above tests have been universally unrewarding when applied to aborted, mummified, or stillborn piglets.

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374 Metabolic response of pigs to Porcine Reproductive and Respiratory Syndrome virus infection and nutrient restriction

Journal of Animal Science ◽

10.1093/jas/skz122.104 ◽

2019 ◽

Vol 97 (Supplement_2) ◽

pp. 57-57

Author(s):

Emma T Helm ◽

Shelby Curry ◽

Wesley Schweer ◽

Carson De Mille ◽

Eric R Burrough ◽

...

Keyword(s):

Skeletal Muscle ◽

Virus Infection ◽

Feed Intake ◽

Liver Glycogen ◽

Nutrient Restriction ◽

Treatment Groups ◽

Prrs Virus ◽

Ad Libitum ◽

Glycogen Stores ◽

Tissue Accretion

Abstract Porcine reproductive and respiratory syndrome (PRRS) virus is one of the most economically significant pig pathogens worldwide. The virus infects pigs at all production stages and significantly reduces the tissue accretion of growing pigs. However, the metabolic explanation for these reductions in tissue accretion remain poorly defined. Additionally, PRRS virus infection is often accompanied by reductions in feed intake, making it difficult to discern which effects are virus versus feed intake driven. To account for this, a pair-fed model was employed to examine the effects of PRRS infection and nutrient restriction on skeletal muscle and liver metabolism. Forty-eight pigs were randomly selected (11.34 ± 1.54 kg BW) and allotted to 3 treatments (n = 16 pigs/treatment): 1) PRRS naïve, ad libitum fed (Ad), 2) PRRS-inoculated, ad libitum fed (PRRS+), and 3) PRRS naïve, pair-fed to the PRRS-inoculated pigs’ daily feed intake (PF). At dpi 10 and dpi 17, 8 pigs per treatment were euthanized and tissues collected. Tissues were assayed for markers of proteolysis [longissimus skeletal muscle (LM) only], oxidative stress (LM only), and glycogen levels (LM and liver). Markers of LM proteolysis (calpain, 20s proteasome, caspase 3/7 activities) and mitochondrial reactive oxygen species production did not differ (P > 0.10) between treatment groups at either timepoint. Liver glycogen stores were reduced (P < 0.001) in PRRS+ pigs compared with both Ad and PF pigs, which did not differ from each other. Muscle glycogen did not differ (P > 0.10) between treatment groups. However, liver glycogen stores were completely depleted due to PRRS+, but not pair-feeding, indicating that liver glycogen stores and glucose are preferentially utilized by pigs to produce and support immune components. These data suggest that even under severe viral challenge and feed restriction, the pig does not upregulate LM proteolysis to re-allocate nutrients to fuel the immune response.

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Identification of a putative quantitative trait nucleotide in guanylate binding protein 5 for host response to PRRS virus infection

BMC Genomics ◽

10.1186/s12864-015-1635-9 ◽

2015 ◽

Vol 16 (1) ◽

Cited By ~ 51

Author(s):

James E. Koltes ◽

Eric Fritz-Waters ◽

Chris J. Eisley ◽

Igseo Choi ◽

Hua Bao ◽

...

Keyword(s):

Virus Infection ◽

Quantitative Trait ◽

Host Response ◽

Binding Protein ◽

Quantitative Trait Nucleotide ◽

Prrs Virus ◽

Guanylate Binding Protein

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The 40 kDa Linear Polyethylenimine Inhibits Porcine Reproductive and Respiratory Syndrome Virus Infection by Blocking Its Attachment to Permissive Cells

Viruses ◽

10.3390/v11090876 ◽

2019 ◽

Vol 11 (9) ◽

pp. 876 ◽

Cited By ~ 2

Author(s):

Jie Wang ◽

Jie Li ◽

Nana Wang ◽

Qi Ji ◽

Mingshuo Li ◽

...

Keyword(s):

Virus Infection ◽

Infectious Diseases ◽

Broad Spectrum ◽

Alveolar Macrophages ◽

Cultured Cells ◽

Cationic Polymer ◽

Respiratory Syndrome Virus ◽

Minimal Effect ◽

Prrs Virus ◽

Linear Polyethylenimine

Porcine reproductive and respiratory syndrome (PRRS) is one of the most economically devastating infectious diseases in pigs worldwide. The causative agent is the PRRS virus (PRRSV). In this study, we explored polyethylenimine (PEI), a cationic polymer with different forms (linear or branched), to inhibit the replication of PRRSV. Our results demonstrate that the linear but not the 40 kDa branched PEI, or the 25 kDa linear PEI, were well tolerated in cultured cells and exhibited a broad-spectrum inhibition of heterogeneous PRRSV-2 isolates in both MARC-145 cells and primary porcine pulmonary alveolar macrophages (PAMs). Further analysis suggests that PEI could prevent the attachment of PRRSV virions to the susceptible cells. Notably, PEI had a minimal effect on PRRSV internalization in MARC-145 cells, whereas PEI promoted the internalization of PRRSV virions in PAMs, which suggests that these two types of cells might have different internalization processes of PRRSV virions. In conclusion, our data demonstrate that PEI could be used as a novel inhibitor against PRRSV.

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