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Acquired immunity and vaccination against infectious pancreatic necrosis virus of salmon
•Humoral response, specifically IgM correlate with vaccine protection against IPNV infections.•Kinetics of CD4+ and CD8+ T-cell gene expression correlate with protection against IPN.•Inactivated whole virus vaccines eliciting an antibody titer of ⩾1.40 OD490 at challenge are protective.•High antibod...
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Published in: | Developmental and comparative immunology 2014-04, Vol.43 (2), p.184-196 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | •Humoral response, specifically IgM correlate with vaccine protection against IPNV infections.•Kinetics of CD4+ and CD8+ T-cell gene expression correlate with protection against IPN.•Inactivated whole virus vaccines eliciting an antibody titer of ⩾1.40 OD490 at challenge are protective.•High antibody levels prevent dissemination and the seeding of virus in target organs.
Acquired immunity plays an important role in the protection of salmonids vaccinated against infectious pancreatic necrosis virus (IPNV) infections. In recent years, vaccine research has taken a functional approach to find the correlates of protective immunity against IPNV infections. Accumulating evidence suggests that the humoral response, specifically IgM is a correlate of vaccine protection against IPNV infections. The role of IgT on the other hand, especially at the sites of virus entry into the host is yet to be established. The kinetics of CD4+ and CD8+ T-cell gene expression have also been shown to correlate with protection in salmonids, suggesting that other arms of the adaptive immune response e.g. cytotoxic T cell responses and Th1 may also be important. Overall, the mechanisms of vaccine protection observed in salmonids are comparable to those seen in other vertebrates suggesting that the immunological basis of vaccine protection has been conserved across vertebrate taxa. |
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ISSN: | 0145-305X 1879-0089 |
DOI: | 10.1016/j.dci.2013.08.008 |