Variation in resistance to the Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) in Pietrain and Miniature pigs

Abstract

Porcine reproductive and respiratory syndrome (PRRS) is one of the economically most important diseases of swine. Viraemia and the prolonged persistence of the virus are among the most critical factors. Virus replication and severity of disease vary with virus isolates, and there is rising evidence for a genetic component of the host susceptibility. Dissecting the genetic basis of resistance/susceptibility to PRRS virus (PRRSV) might lead to improved knowledge on the molecular mechanisms of PRRS and the establishment of genetic markers for future disease control. The aim of this study was to establish a porcine model with emphasized genetic differences in PRRSV susceptibility. Seven 'Wiesenauer Miniature' pigs (MI), a local German breed and eight commercial Pietrain (PI) pigs were challenged with 10(5) TCID(50) of an attenuated PRRSV strain (Ingelvac PRRSV MLV). Clinical status, viraemia and seroconversion of the pigs were compared. No clinical signs were observed during the experiment. Viraemia peaked on day 6 p.i., with 100% of viraemic pigs in PI and on day 12 p.i with 87% of viraemic MI. Viraemia lasted for up to 35 days in MI and for at least 72 days in PI. This surprising result was confirmed by a second study with another four MI. MI and PI showed maximum virus titres of 10(2.5) TCID(50)/ml of serum and 10(4.5) TCID(50)/ml, respectively, indicating a virus replication in MI of approximately 3.3% that of PI over the complete period. MI were more efficient in antibody production. With such pronounced breed differences, the model is of high relevance for the genetic dissection of PRRS pathogenesis and susceptibility.

Integrative Model of the Immune Response to a Pulmonary Macrophage Infection: What Determines the Infection Duration?

“…Few experimental studies focus on the response variability due to the viral strain or pig breed susceptibility. In a resistant pig breed, the viral load was around 35 days in the sera (estimated around 56 days in the lung) [52] and around 52 days in the lung with a low virulent strain [62]. Conversely, a more susceptible pig breed showed a 72-day viremia (estimated around 115 days in the lung) [52].…”

“…The highly virulent strains are associated with a prolonged viremia, a high viral replication rate and a high humoral response [50]. Moreover, the genetic component of the host susceptibility to PRRSv has been demonstrated [51], [52]. Pig susceptibility can also depend on other factors such as herd management.…”

“…Pig susceptibility can also depend on other factors such as herd management. The more susceptible pigs develop prolonged viremia, with low titers of neutralising antibodies [10], [52], probably linked to a high macrophage permissiveness and/or specific cytokine profiles [51].…”

Microbiome associations in pigs with the best and worst clinical outcomes following co-infection with porcine reproductive and respiratory syndrome virus (PRRSV) and porcine circovirus type 2 (PCV2)

“…A significant difference between the two groups was shown on 28 dpi, when mean PRRSV viremia was 2.46 and 0.86 log 10 copies/PCR reaction for the worst and best outcome groups, respectively (p = 0.015, unpaired t-test). After the initial decay, rebound peaks were observed in several pigs, a phenomenon initially described in 2010 (Reiner et al, 2010) and later by us (Boddicker et al, 2012). Another way to present infection is through the calculation of virus load or the area under the viremia curve (Boddicker et al, 2012).…”

A WUR SNP is associated with European Porcine Reproductive and Respiratory Virus Syndrome resistance and growth performance in pigs

“…Thus, Meishan and Large White pigs seem to be more resistant to the effects of the virus than Duroc and Pietrain pigs (Petry et al, 2005(Petry et al, , 2007Reiner et al, 2010). More recently, the heritability for viral load was estimated to be close to 0.3 after challenge with a North American PRRSV strain (Boddicker et al, 2012).…”