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Vaccine genotype and route of administration affect pseudorabies field virus latency load after challenge
Institution:3. Division of Oncology Research, Mayo Clinic, Rochester, Minnesota 55905;4. Departments of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, Minnesota 55905;5. Departments of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota 55905;1. School of Chemistry and Molecular Bioscience, The University of Queensland, QLD, 4072, Australia;2. Centre for Kidney Disease-Venomics Research, School of Medicine, The University of Queensland, Level 5, 37 Kent Street, Woolloongabba, QLD, 4102, Australia;3. The University of Queensland, UQ Centre for Clinical Research, Brisbane, QLD, 4029, Australia;4. Venom Science Pty Ltd, Tanunda South Australia, 5352, Australia;3. Departments of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul 137-701, South Korea;4. Department of Molecular Science and Technology, Ajou University, Suwon 443-749, South Korea,;5. Laboratory of Genetics, Intramural Research Program, NIA, National Institutes of Health, Baltimore, Maryland 21224;6. Department of Physiology, Graduate School of Medicine, Keio University, Shinjuku, Tokyo 160-8582, Japan;3. Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15219;4. Department of Microbiology and Immunology, The Geisel School of Medicine at Dartmouth, Hanover, New Hampshire 03755;5. Department of Immunology, Roswell Park Cancer Institute, Buffalo, New York 14263;3. Research Center for Women''s Disease, Department of Life Systems, Sookmyung Women''s University, Seoul 140-742, Republic of Korea;4. Research Center for Cell Fate Control, College of Pharmacy, Sookmyung Women''s University, Seoul 140-742, Republic of Korea
Abstract:The influence of vaccine genotype and route of administration on the efficacy of pseudorabies virus (PRV) vaccines against virulent PRV challenge was evaluated in a controlled experiment using five genotypically distinct modified live vaccines (MLVs) for PRV. Several of these MLVs share deletions in specific genes, however, each has its deletion in a different locus within that gene. Pigs were vaccinated with each vaccine, either via the intramuscular or intranasal route, and subsequently challenged with a highly virulent PRV field strain. During a 2-week period following challenge with virulent PRV, each of the vaccine strains used in this study was evaluated for its effectiveness in the reduction of clinical signs, prevention of growth retardation and virulent virus shedding. One month after challenge, tissues were collected and analyzed for virulent PRV latency load by a recently developed method for the electrochemiluminescent quantitation of latent herpesvirus DNA in animal tissues after PCR amplification. It was determined that all vaccination protocols provided protection against clinical signs resulting from field virus challenge and reduced both field virus shedding and latency load after field virus challenge. Our results indicated that vaccine efficacy was significantly influenced by the modified live vaccine strain and route of administration. Compared to unvaccinated pigs, vaccination reduced field virus latency load in trigeminal ganglia, but significant differences were found between vaccines and routes of administration. We conclude that vaccine genotype plays a role in the effectiveness of PRV MLVs.
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