Evaluation of a 20 year old porcine reproductive and respiratory syndrome (PRRS) modified live vaccine (Ingelvac ® PRRS MLV) against two recent type 2 PRRS virus isolates in South Korea

Jeong, Jiwoon; Choi, Kyuhyung; Kang, Il Jun; Park, Changhoon; Chae, Chanhee

doi:10.1016/j.vetmic.2016.07.006

Cited by 27 publications

(29 citation statements)

References 40 publications

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“…The lung lesion scores and PRRSV antigens in lung tissues were significantly reduced in the vaccination groups compared to the unvaccinated group after challenge with heterologous viruses [15][16][17][18] . Our results are in agreement with those of a previous single challenge study that demonstrated partial cross-protection by PRRSV MLV 15, 16,22,[41][42][43][44] . On the other hand, our cross-protection results are in contrast with those of another previous dual-challenge study in which vaccination with PRRSV-1 MLV reduced only PRRSV-1 viremia and not PRRSV-2 viremia 45 .…”

Section: Discussionsupporting

confidence: 93%

Cell-mediated immune response and protective efficacy of porcine reproductive and respiratory syndrome virus modified-live vaccines against co-challenge with PRRSV-1 and PRRSV-2

Madapong

Saeng‐chuto

Boonsoongnern

et al. 2020

Sci Rep

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Cell-mediated immunity (CMI), IL-10, and the protective efficacy of modified-live porcine reproductive and respiratory syndrome virus (PRRSV) vaccines (MLV) against co-challenge with PRRSV-1 and PRRSV-2 (HP-PRRSV) were investigated. Seventy, PRRSV-free, 3-week old, pigs were allocated into 7 groups. Six groups were intramuscularly vaccinated with MLV, including Porcilis (PRRSV-1 MLV, MSD Animal Health, The Netherlands), Amervac (PRRSV-1 MLV, Laboratorios Hipra, Spain), Fostera (PRRSV-2 MLV, Zoetis, USA), Ingelvac PRRS MLV and Ingelvac PRRS ATP (PRRSV-2, Boehringer Ingelheim, USA), and Prime Pac PRRS (PRRSV-2 MLV, MSD Animal Health, The Netherlands). Unvaccinated pigs were left as control. Lymphocyte proliferative response, IL-10 and IFN-γ production were determined. At 35 days post-vaccination (DPV), all pigs were inoculated intranasally with 2 ml of each PRRSV-1 (10 5.4 tciD 50 /ml) and PRRSV-2 (10 5.2 tciD 50 /ml, HP-PRRSV). Following challenge, sera were quantitatively assayed for PRRSV RNA. Pigs were necropsied at 7 days post-challenge. Viremia, macro-and microscopic lung lesion together with pRRSV antigen presence were evaluated in lung tissues. The results demonstrated that, regardless of vaccine genotype, CMI induced by all MLVs was relatively slow. Increased production of IL-10 in all vaccinated groups was observed at 7 and 14 DPV. Pigs in Amervac, Ingelvac MLV and Ingelvac ATP groups had significantly higher levels of IL-10 compared to Porcilis, Fostera and Prime Pac groups at 7 and 14 DPV. Following challenge, regardless to vaccine genotype, vaccinated pigs had significantly lower lung lesion scores and PRRSV antigens than those in the control group. Both PRRSV-1 and PRRSV-2 RNA were significantly reduced. Prime Pac pigs had lowest PRRSV-1 and PRRSV-2 RNA in serum, and micro-and macroscopic lung lesion scores (p < 0.05) compared to other vaccinated groups. In conclusion, PRRSV MLVs, regardless of vaccine genotype, can reduce viremia and lung lesions following co-challenge with PRRSV-1 and PRRSV-2 (HP-PRRSV). The main difference between PRRSV MLV is the production of IL-10 following vaccination. Porcine reproductive and respiratory syndrome (PRRS) is a devastating disease in pigs characterized by reproductive and respiratory failures. PRRS virus (PRRSV), an enveloped, positive-sense single-stranded RNA virus belonging to the Arteriviridae family, order Nidovirales, is the causative agent 1. Two antigenically distinct genotypes of PRRSV, PRRSV-1 and PRRSV-2, have been recognized. The genomes of both genotypes are 15 kb in

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Section: Discussionsupporting

confidence: 93%

Cell-mediated immune response and protective efficacy of porcine reproductive and respiratory syndrome virus modified-live vaccines against co-challenge with PRRSV-1 and PRRSV-2

Madapong

Saeng‐chuto

Boonsoongnern

et al. 2020

Sci Rep

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“…PRRSV-2 vaccinated pigs were almost completely protected from viremia following challenge with the homologous PRRSV-2 strain which is in accordance with previous studies with this vaccine [5,[31][32][33]. In contrast, vaccination with the PRRSV-2 vaccine had limited effect on viremia following challenge with PRRSV-1 which also is in accordance with the outcome of most of the previous comparable studies with this vaccine [5,26,34].…”

Section: Discussionsupporting

confidence: 90%

Efficacy and safety of simultaneous vaccination with two modified live virus vaccines against porcine reproductive and respiratory syndrome virus types 1 and 2 in pigs

Kristensen

Kvisgaard

Pawłowski

et al. 2018

Vaccine

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“…As an RNA virus, PRRSV is prone to mutation, leading to genetic diversity within genotypes over time (10). Mutation and recombination are two common evolutionary mechanisms for PRRSV, which can cause enhanced fitness for survival or increased virulence (11).…”

mentioning

confidence: 99%

Heparanase Upregulation Contributes to Porcine Reproductive and Respiratory Syndrome Virus Release

Guo

Zhu

Guo

et al. 2017

J Virol

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Porcine reproductive and respiratory syndrome virus (PRRSV) continues to cause substantial economic losses to the pig industry worldwide. Heparan sulfate (HS) is used by PRRSV for initial attachment to target cells. However, the role of HS in the late phase of PRRSV infection and the mechanism of virus release from host cells remain largely unknown. In this study, we showed that PRRSV infection caused a decrease in HS expression and upregulated heparanase, the only known enzyme capable of degrading HS. We subsequently demonstrated that the NF-B signaling pathway and cathepsin L protease were involved in regulation of PRRSV infectioninduced heparanase. In addition, we found that ablation of heparanase expression using small interfering RNA duplexes increased cell surface expression of HS and suppressed PRRSV replication and release, whereas overexpression of heparanase reduced HS surface expression and enhanced PRRSV replication and release. These data suggest that PRRSV activates NF-B and cathepsin L to upregulate and process heparanase, and then the active heparanase cleaves HS, resulting in viral release. Our findings provide new insight into the molecular mechanism of PRRSV egress from host cells, which might help us to further understand PRRSV pathogenesis.IMPORTANCE Porcine reproductive and respiratory syndrome virus (PRRSV) causes great economic losses each year to the pig industry worldwide. The molecular mechanism of PRRSV release from host cells largely remains a mystery. In this study, we demonstrate that PRRSV activates NF-B and cathepsin L to upregulate and process heparanase, and then the active heparanase is released to the extracellular space and exerts enzymatic activity to cleave heparan sulfate, resulting in viral release. Our findings provide new insight into the molecular mechanism of PRRSV egress from host cells, which might help us to further understand PRRSV pathogenesis.KEYWORDS PRRSV, heparan sulfate, heparanase, viral release, porcine reproductive and respiratory syndrome virus P orcine reproductive and respiratory syndrome (PRRS) has become one of the most important diseases of intensive pig production worldwide since its emergence in the late 1980s (1, 2). This disease is characterized by respiratory disease, weight loss, and poor growth performance, as well as by late-term abortions (3). The causative agent, PRRS virus (PRRSV), is a small, enveloped, positive-sense, single-stranded RNA virus of the genus Arterivirus, in the family Arteriviridae within the order Nidovirales (4, 5). The PRRSV genome is approximately 15 kb in length and consists of at least 12 overlapping open reading frames (6, 7). Due to the genetic and antigenic differences, PRRSV can be divided into European genotype 1 and North American genotype 2, with Lelystad and VR-2332 as prototypical strains, respectively, which share about 60% nucleotide sequence identity (8). In 2006, highly pathogenic PRRSV (HP-PRRSV)

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Evaluation of a 20 year old porcine reproductive and respiratory syndrome (PRRS) modified live vaccine (Ingelvac ® PRRS MLV) against two recent type 2 PRRS virus isolates in South Korea

Cited by 27 publications

References 40 publications

Cell-mediated immune response and protective efficacy of porcine reproductive and respiratory syndrome virus modified-live vaccines against co-challenge with PRRSV-1 and PRRSV-2

Cell-mediated immune response and protective efficacy of porcine reproductive and respiratory syndrome virus modified-live vaccines against co-challenge with PRRSV-1 and PRRSV-2

Efficacy and safety of simultaneous vaccination with two modified live virus vaccines against porcine reproductive and respiratory syndrome virus types 1 and 2 in pigs

Heparanase Upregulation Contributes to Porcine Reproductive and Respiratory Syndrome Virus Release

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