Pathogenicity of three type 2 porcine reproductive and respiratory syndrome virus strains in experimentally inoculated pregnant gilts

Ladinig, Andrea; Detmer, Susan E.; Clarke, Kyle; Ashley, Carolyn; Rowland, Raymond R. R.; Lunney, Joan K.; Harding, John C. S.

doi:10.1016/j.virusres.2015.03.005

Cited by 35 publications

(38 citation statements)

References 46 publications

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“…A second generation of 5 PHGC trials involved experimental infection of similar lines of pigs with the more recent KS-2006-72109 PRRSV strain, which is 89% identical to the NVSL 97 strain at the viral GP5 peptide sequence level (Ladinig et al, 2015).…”

Section: Prrs Host Genomics Consortium Prrsv Infection Trialsmentioning

confidence: 99%

Host genetics of response to porcine reproductive and respiratory syndrome in nursery pigs

Dekkers

Rowland

Lunney

et al. 2017

Veterinary Microbiology

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A B S T R A C TPRRS is the most costly disease in the US pig industry. While vaccination, biosecurity and eradication effort have had some success, the variability and infectiousness of PRRS virus strains have hampered the effectiveness of these measures. We propose the use of genetic selection of pigs as an additional and complementary effort. Several studies have shown that host response to PRRS infection has a sizeable genetic component and recent advances in genomics provide opportunities to capitalize on these genetic differences and improve our understanding of host response to PRRS. While work is also ongoing to understand the genetic basis of host response to reproductive PRRS, the focus of this review is on research conducted on host response to PRRS in the nursery and grow-finish phase as part of the PRRS Host Genetics Consortium. Using experimental infection of large numbers of commercial nursery pigs, combined with deep phenotyping and genomics, this research has identified a major gene that is associated with host response to PRRS. Further functional genomics work identified the GBP5 gene as harboring the putative causative mutation. GBP5 is associated with innate immune response. Subsequent work has validated the effect of this genomic region on host response to a second PRRSV strain and to PRRS vaccination and co-infection of nursery pigs with PRRSV and PCV2b. A genetic marker near GBP5 is available to the industry for use in selection. Genetic differences in host response beyond GBP5 appear to be highly polygenic, i.e. controlled by many genes across the genome, each with a small effect. Such effects can by capitalized on in a selection program using genomic prediction on large numbers of genetic markers across the genome. Additional work has also identified the genetic basis of antibody response to PRRS, which could lead to the use of vaccine response as an indicator trait to select for host response to PRRS. Other genomic analyses, including gene expression analyses, have identified genes and modules of genes that are associated with differences in host response to PRRS and can be used to further understand and utilize differences in host response. Together, these results demonstrate that genetic selection can be an additional and complementary tool to combat PRRS in the swine industry.

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Section: Prrs Host Genomics Consortium Prrsv Infection Trialsmentioning

confidence: 99%

Host genetics of response to porcine reproductive and respiratory syndrome in nursery pigs

Dekkers

Rowland

Lunney

et al. 2017

Veterinary Microbiology

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“…In non-pregnant sows, PRRS can develop without symptoms, or cause appetite loss or fever [6]. In pregnant sows, the virus may cross the placenta during late gestation, infect developing foetuses and increase the risk of abortion, early farrowing and foetal death [8, 9]. Neonatal and nursery pigs may experience respiratory distress, listlessness, pneumonia, high fever, anorexia, conjunctivitis and growth retardation [6, 10–12].…”

Section: Introductionmentioning

confidence: 99%

Control and eradication of porcine reproductive and respiratory syndrome virus type 2 using a modified-live type 2 vaccine in combination with a load, close, homogenise model: an area elimination study

Rathkjen

Dall²

2017

Acta Vet Scand

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BackgroundPorcine reproductive and respiratory syndrome virus (PRRSV) causes significant animal and economic losses worldwide. The infection is difficult to control and PRRSV elimination at local level requires coordinated intervention among multiple farms. This case study describes a successful elimination of PRRSV from all 12 herds on the Horne Peninsula, Denmark, using a combination of load, close, homogenise (LCH) using PRRSV type 2 modified-live vaccine, optimised pig flow, and’10 Golden Rules’ (10GR) for biosecurity management. To the authors’ knowledge, this is the first successful European PRRSV area elimination project documented in detail. The PRRSV type 2 modified-live vaccine was used as part of the LCH method in breeding herds. Complete or partial depopulation was performed in some infected herds. A simplified biosecurity protocol (10GR) based on the McREBEL™ system of pig flow management, was employed in all herds and at all times throughout the study.ResultsAt study commencement, all herds were infected with PRRSV, and most were actively shedding virus. In just over 18 months, all 12 herds on the Horne Peninsula were confirmed to be PRRSV negative by polymerase chain reaction testing and negative for antibodies against PRRSV by enzyme–linked immunosorbent assay testing. All herds were subsequently obtained ‘Specific Pathogen Free’ status for PRRSV.ConclusionsThis study provides compelling evidence suggesting that an area elimination plan combining LCH with PRRSV type 2 vaccination, optimised pig flow, and 10GR for biosecurity management can effectively eliminate PRRSV from a geographic area. Additionally this study confirms the value of a previously unpublished, simplified alternative to the McREBEL system for controlling PRRSV.Electronic supplementary materialThe online version of this article (doi:10.1186/s13028-016-0270-z) contains supplementary material, which is available to authorized users.

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“…Several studies have shown that the duration of viraemia varied depending on the PRRSV strain and on the age of the animal (Diaz et al., ). Viraemia was reported as early as 24 hr post‐infection to 1 month with wide variations in onset, peak viraemia between 7 and 14 days (Ladinig et al., ; Rossow et al., ). Clearance of viraemia has been attributed to both cell‐mediated immune responses and onset of neutralizing antibodies during the 3rd week post‐PRRSV infection (Diaz et al., ; Lopez & Osorio, ).…”

Section: Discussionmentioning

confidence: 99%

Pathogenic characterization of porcine reproductive and respiratory syndrome virus of Indian origin in experimentally infected piglets

Senthilkumar

Rajukumar

Kumar

et al. 2018

Transbound Emerg Dis

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Porcine reproductive and respiratory syndrome (PRRS) is an economically important transboundary viral disease of pigs confronting the swine industry worldwide. This study was aimed to assess the pathogenic potential of PRRS virus belonging to genotype 2 that emerged in India in 2013. Nine 6-week-old piglets were inoculated intranasally with 2 × 10 TCID /ml of PRRSV (Ind-297221/2013). Three piglets were kept as uninfected controls. Blood and nasal swabs were collected daily up to 7 days post-infection (dpi) and on alternate days subsequently. Piglets were necropsied for tissue sample collection either on death or after euthanasia on 7, 14 or 21 dpi (one uninfected control and three PRRSV-infected piglets per interval). The virus caused high fever, typical blue ear, weight loss, respiratory distress, diarrhoea and leucopenia between 2 and 8 dpi. Two infected piglets died (on 3 and 17 dpi) during the course of study. The presence of virus in serum and nasal secretion was observed up to 19 and 17 dpi, respectively, with the maximum load between 4 and 7 dpi. Seroconversion started 6 dpi and the mean PRRSV antibody titre reached up to 640 by 21 dpi. Virus load was highest in tonsils at all the intervals, whereas in spleen and lymph nodes load was higher in later intervals. Major microscopic lesions in PRRSV-infected piglets included moderate to severe interstitial pneumonia, lymphoid depletion in tonsils and lymph nodes (cystic), thymic atrophy, reactive hyperplasia followed by lymphoid depletion in spleen. PRRSV antigen was consistently demonstrated by immunoperoxidase test in the lungs, spleen, tonsils and lymph nodes. Antigen distribution was more widespread on 7 and 14 dpi than on 21 dpi. The findings establish that the Indian PRRSV is highly pathogenic to piglets.

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Pathogenicity of three type 2 porcine reproductive and respiratory syndrome virus strains in experimentally inoculated pregnant gilts

Cited by 35 publications

References 46 publications

Host genetics of response to porcine reproductive and respiratory syndrome in nursery pigs

Host genetics of response to porcine reproductive and respiratory syndrome in nursery pigs

Control and eradication of porcine reproductive and respiratory syndrome virus type 2 using a modified-live type 2 vaccine in combination with a load, close, homogenise model: an area elimination study

Pathogenic characterization of porcine reproductive and respiratory syndrome virus of Indian origin in experimentally infected piglets

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