Comparison of the Pathogenicity of Two US Porcine Reproductive and Respiratory Syndrome Virus Isolates with that of the Lelystad Virus

Halbur, Patrick G.; Paul, P. S.; Frey, M. L.; Landgraf, John; Eernisse, K. A.; Meng, Xiang‐Jin; Andrews, John J.; Lum, Melissa A.; Rathje, J. A.

doi:10.1177/030098589503200606

Cited by 601 publications

(579 citation statements)

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“…The variation in pathogenesis of different isolates of PRRSV is well documented [20,32,35]. Pathological studies have led workers to postulate that it is related to their ability to replicate in vivo [33] though it is possible that such pathogenesis may also be related in part to the ability of certain strains to evade or modify the immune system of the host.…”

Section: Discussionmentioning

confidence: 99%

A review of evidence for immunosuppression due to Porcine Reproductive and Respiratory Syndrome Virus

Drew¹

2000

Vet. Res.

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-Accounts of field disease and experimental studies involving porcine reproductive and respiratory syndrome (PRRS) are reviewed for evidence of immunomodulation or immunosuppression by the causative virus. The conclusion is that immunomodulation through infection of alveolar macrophages is likely to occur, but that it is transient and at a local level, in the lung. There is some evidence for more subtle effects via more disseminated replication or induction of apoptosis with some isolates, but more definitive studies are needed. There is some emerging evidence of interaction between PRRSV and different cells of the immune system, but its significance for the course of disease or pig health are unclear. Likewise, the current experimental evidence for any interaction of PRRSV with other pathogens is ambiguous and therefore no firm conclusions can yet be drawn. Strains of PRRSV do vary in pathogenicity, which may be related to their degree of ability to cause overt respiratory disease in the absence of other agents. Experimentally, varying degrees of interstitial pneumonia are a common histological finding. There is, as yet, no firm evidence of general immunosuppression -in fact, some contrary evidence exists in the form of observations of a transient enhancement of humoral response, possibly through polyclonal B cell activation. The basis of pathogenicity of PRRSV and of any interaction with other agents is still unknown and is likely to remain unclear. Virus interaction with the pig's immune system must be addressed before any assessment of virulence of any known or emergent strains of PRRSV can be made. swine disease / PRRSV / coronaviridae / nidovirales / arterivirus / viral immunomodulation / pig Résumé -Immunosuppression due au virus du syndrome dysgénésique et respiratoire porcin : le point sur les résultats. Une revue bibliographique de rapports de terrain et expérimentaux impliquant le syndrome dysgénésique et respiratoire du porc (PRRS) a permis de faire le point sur les résultats montrant une immunomodulation ou une immunosuppression dues au virus. La conclusion est qu'il est possible que l'infection des macrophages alvéolaires provoque une immunomodulation, mais celle-ci reste transitoire et localisée dans les poumons. Certains résultats suggèrent des effets plus subtils avec certaines souches, faisant intervenir une réplication plus disséminée ou Vet. Res. 31 (2000) 27-39 27 © INRA, EDP Sciences

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Section: Discussionmentioning

confidence: 99%

A review of evidence for immunosuppression due to Porcine Reproductive and Respiratory Syndrome Virus

Drew¹

2000

Vet. Res.

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“…Fifty percent endpoint titers were computed by the Reed-Meunch method [25]. The presence of macroscopic lung lesions for all seven lung lobes was examined and scored as previously described [26]. All animal studies were conducted in accordance with the National Animal Disease Center's Institutional Animal Care and Use Committee.…”

Section: Experimental Designmentioning

confidence: 99%

Vaccination with NS1-truncated H3N2 swine influenza virus primes T cells and confers cross-protection against an H1N1 heterosubtypic challenge in pigs

Kappes

Sandbulte

Platt

et al. 2012

Vaccine

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The diversity of contemporary swine influenza virus (SIV) strains impedes effective immunization of swine herds. Mucosally delivered, attenuated virus vaccines are one approach with potential to provide broad crossprotection. Reverse genetics-derived H3N2 SIV virus with truncated NS1 (NS1Δ126 TX98) is attenuated and immunogenic when delivered intranasally in young pigs. We analyzed T-cell priming and cross-protective efficacy in weanling piglets after intranasal inoculation with NS1Δ126 TX98 versus wild type TX98. In vivo replication of the truncation mutant was minimal compared to the wild type virus. T-cell responses were greater in magnitude in pigs infected with the wild type virus in in vitro restimulation assays. According to the expression of activation marker CD25, peripheral T cell recall responses in NS1Δ126 TX98 infected pigs were minimal. However, intracellular IFN-γ data indicate that the attenuated virus induced virus-specific CD4 + CD8 -, CD4 + CD8 + , CD4 -CD8 + , and γδ T cells within 28 days. The IFN-γ response appeared to contract, as responses were reduced at later time points prior to challenge. CD4 + CD8 + cells isolated 5 days after heterosubtypic H1N1 challenge (day 70 overall) showed an elevated CD25 response to virus restimulation. Pigs previously infected with wild type TX98 were protected from replication of the H1N1 challenge virus. Vaccination with NS1Δ126 TX98 was associated with significantly lower levels of Th1-associated cytokines in infected lungs but provided partial cross-protection against the H1N1 challenge. These results demonstrate that NS1Δ SIV vaccines can elicit cell-mediated cross-protection against antigenically divergent strains. The diversity of contemporary swine influenza virus (SIV) strains impedes effective immunization of swine herds. Mucosally delivered, attenuated virus vaccines are one approach with potential to provide broad cross-protection. Reverse genetics-derived H3N2 SIV virus with truncated NS1 (NS1 126 TX98) is attenuated and immunogenic when delivered intranasally in young pigs. We analyzed T-cell priming and cross-protective efficacy in weanling piglets after intranasal inoculation with NS1 126 TX98 versus wild type TX98. In vivo replication of the truncation mutant was minimal compared to the wild type virus. T-cell responses were greater in magnitude in pigs infected with the wild type virus in in vitro restimulation assays. According to the expression of activation marker CD25, peripheral T cell recall responses in NS1 126 TX98 infected pigs were minimal. However, intracellular IFN-␥ data indicate that the attenuated virus induced virus-specific CD4 + CD8 -, CD4 + CD8 + , CD4 -CD8 + , and ␥␦ T cells within 28 days. The IFN-␥ response appeared to contract, as responses were reduced at later time points prior to challenge. CD4 + CD8 + cells isolated 5 days after heterosubtypic H1N1 challenge (day 70 overall) showed an elevated CD25 response to virus restimulation. Pigs previously infected with wild type TX98 were protected from replicatio...

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“…* Corresponding author: peter.delputte@UGent.be problems in pigs of all ages, in combination with other pathogens [7,8,21,28]. In vivo, PRRSV has a predilection for differentiated macrophages [18,44].…”

Section: Introductionmentioning

confidence: 99%

Involvement of proteases in porcine reproductive and respiratory syndrome virus uncoating upon internalization in primary macrophages

2008

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-Porcine reproductive and respiratory syndrome virus (PRRSV) replicates in differentiated macrophages. In macrophages, heparan sulphate glycosaminoglycans mediate the initial PRRSV attachment and the receptor sialoadhesin mediates both PRRSV attachment and internalization into endosomes. Upon a pH drop, PRRSV is uncoated and its genome is released from the endosomes into the cytoplasm, which allows virus replication. However, expression of heparan sulphate and sialoadhesin in non-susceptible cells only allows virus internalization, but no virus uncoating and infection, indicating that other factors are involved. In the present study, it is shown that treatment of macrophages with serum (mainly the alpha-globulin fraction) inhibited PRRSV infection without affecting attachment and internalization. Because alpha-globulins contain several protease inhibitors, macrophages were treated with different protease inhibitors to investigate the involvement of proteases in PRRSV uncoating. Treatment of macrophages with broadly active inhibitors of serine or aspartic proteases, but not cysteine-or metallo-proteases, inhibited PRRSV uncoating and infection. Further investigation using specific inhibitors indicated that the aspartic protease cathepsin E is involved during PRRSV uncoating, but did not allow identification of the serine protease involved. The involvement of cathepsin E during PRRSV uncoating was confirmed by partial co-localization of internalized PRRSV with cathepsin E. Furthermore, cathepsin E expression increased with macrophage cultivation, which was positively correlated with an increased susceptibility to PRRSV infection. Together, these data show that, in macrophages, both the aspartic protease cathepsin E and an unidentified trypsin-like serine protease are involved in uncoating of internalized PRRSV and subsequent infection. porcine arterivirus / macrophage / virus entry / protease / receptor

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Comparison of the Pathogenicity of Two US Porcine Reproductive and Respiratory Syndrome Virus Isolates with that of the Lelystad Virus

Cited by 601 publications

References 20 publications

A review of evidence for immunosuppression due to Porcine Reproductive and Respiratory Syndrome Virus

A review of evidence for immunosuppression due to Porcine Reproductive and Respiratory Syndrome Virus

Vaccination with NS1-truncated H3N2 swine influenza virus primes T cells and confers cross-protection against an H1N1 heterosubtypic challenge in pigs

Involvement of proteases in porcine reproductive and respiratory syndrome virus uncoating upon internalization in primary macrophages

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