SAES-422 Multistate Research Activity Accomplishments Report
Sections
Status: Approved
Basic Information
- Project No. and Title: NC_OLD229 : Porcine Reproductive And Respiratory Syndrome (PRRS): Mechanisms Of Disease And Methods For The Detection, Protection And Elimination of the
- Period Covered: 11/01/2002 to 11/01/2003
- Date of Report: 02/03/2004
- Annual Meeting Dates: 11/07/2003 to 11/08/2003
Participants
[Minutes]
Accomplishments
1. Define molecular and cellular mechanisms of pathogenesis of respiratory and reproductive syndromes caused by PRRSV.
Infectious clones of PRRSV were produced by SD in collaboration with Dr. Dongwan Yoo at Guelph University, Ontario, Canada and also shared with KA. A full-length clone of SD23983 containing a consensus 5end based on Genbank sequences of North American PRRSV strains is currently being tested. The infectious clone of VR2332 reported by Neilsen et al. was generously provided to SD and MO by MN. At MO, two rescue attempts with the VR-2332 clone both resulted in successful recovery of fully infectious virus with cytopathic effect and positive fluorescent-antibody staining indistinguishable from that of other PRRSV isolates. An infectious clone of PRRSV was constructed by NE from a highly abortifacient strain.
New 184 field isolates at MN have regions of radical dissimilarity all through the genome. SD and MN characterized European-like PRRSV isolates identified in the U.S. SD and KA focused on heterogeneity in the Nsp2 gene and a preliminary evaluation of phylogeny of these isolates. The ORF 1 of a European-like PRRSV isolate, SD 01-08, is organized the same as LV. The principal difference was a 17 aa deletion in Nsp2 of SD 01-08 that is not consistently observed. Evolutionary relationships among the European, North American and European-like isolates showed evidence for nucleotide diversity, including several deletions in the Nsp2 region. The European-like PRRSV isolates in the U.S. appear to be from a single Lelystad-like isolate.
KA and SD determined that the ratio of 2b to N in virion preparations was estimated to be approximately 20 N protein molecules for each 2b molecule. Thus 2b is a minor component of the PRRSV virion. KA and Guelph University determined that a single nuclear localization signal (NLS) is involved in the transport of N from the cytoplasm and into nucleus.
VA and IA collaborated on molecular analyses and biological characterizations of PRRSV field reisolates of vaccine and determined that the vaccine-like isolate 98-38803 induces microscopic pneumonia lesions similar in type to, but different in severity and time of onset from, those observed with virulent strains VR2385 and the parent strain of the vaccine.
Quasispecies diversity was analyzed in PRRSV in tonsils from 2 chronically infected farms in IL. All animals in the study harbored multiple, distinct PRRSV variants at both the nucleic acid and amino acid levels. The results indicate that PRRSV exists during natural infection as quasispecies distributions of related genotypes, but that positive natural selection for immune evasiveness in ORF5 does not appear to contribute to maintaining this diversity.
NE and IA conducted studies that indicated genetic variation in susceptibility to PRRSV. Future research with tissues collected will determine which genes are expressed differently in pigs with resistant and susceptible responses to PRRSV.
2. Determine the mechanism(s) and consequences of viral persistence.
NC developed and tested a serologic monitoring method to estimate the point-in-time portion of animals that are resistant to PRRSV, the portion that are susceptible, and the portion of animals that are infective. SD and MN examined the role of lymphoid and non-lymphoid tissue in acute and persistent infections of PRRSV. PRRSV disseminated to most tissues and lymph nodes in 2 d and was detected out to 70 dpi in various tissues. Lymphoid tissues play a prominent role as primary and persistent sites for PRRS viral replication.
MN detected PRRSV in flies in baited jug traps up to 1.66 km from an experimentally infected herd. Hence, transmission and persisttence of PRRSV in swine herds appears to involve flies and mosquitoes. Transport vehicles were also shown to effectively transmit PRRSV, but washing, disinfecting and drying eliminated PRRSV. Drying appeared to be an important component of a transport vehicle sanitation program for PRRSV biosecurity. Aerosolized PRRSV was transported 150 meters in a straight tube model and was infectious to susceptible pigs (MN). Attempts to infect mallard ducks with PRRSV via direct inoculation were not successful.
3. To characterize the different components of the immune response during acute and persistent infection and its implications in diagnostics and pathogenesis.
KA determined that the thymus is the principal site of virus replication in the fetus. IFN gamma and TNF were induced in lung and lymph nodes. IL and USDA-BARC reported an IFN gamma response to PRRSV after 5 weeks. A significant up-regulation of TNF indicated the involvement of innate immunity to PRRSV starting early in the infection, yet there was limited up-regulation of IFN alpha. Co-administration of IFN alpha caused faster returns to pre-vaccination levels for IL-6, IL-8 and IL-10 after 4 weeks. Co-administration of IFN alpha enhanced the IFN gamma response to vaccine. NE and IA produced chimeric mouse X pig anti-PRRSV antibodies that reacted with GP5 in ELISA and Western blot.
MN, NC, and IA collaborated to examine humoral immune responses to structural and nonstructural (nsp) proteins. PRRSV nsp 1, 2, and 4 were cloned. Direct ELISA to nsp 1 revealed that peak levels of antibody exceed anti-PRRSV nucleocapsid (N), and the levels were maintained for at least 120 days. Antibodies to nsp 4 appeared at low levels for a short time.
MN and IA collaborated to report that PRRSV-specific T cell responses were transient and varied substantially among animals. Viral loads decreased 1,000-fold in persistent infections, with tonsil being the primary site of persistence. A weak CMI response appears to contribute to prolonged PRRSV infection and suggests that PRRSV suppresses T cell recognition of infected macrophages. IL monitored the kinetics of the PRRSV-specific IFN gamma response in PBMC for 9 months. A weak IFN gamma response within a few weeks after vaccination appeared to wane at 10 weeks, then rebounded and, with fluctuation, increased gradually in intensity after a period of months without a booster immunization.
IL and NE exposed replacement gilts to a wild-type virus or a heterologous commercial vaccine. A higher IFN gamma response was associated with a lower proportion of stillborn pigs per litter. There was no relationship between humoral or cellular immune response and the recovery of PRRSV from the tonsil. ELISA antibodies were not predictive of any production variables. The use of a heterologous killed PRRS virus vaccine, following exposure to live virus, significantly boosted the cell-mediated immune response.
The role of dendritic cells (DC) in PRRSV pathogenesis and persistence was studied by SD and MN. PRRSV grew in pig DC and reduced expression of MHC class I, CD14, CD11b/c, but not MHC II. MN found no change of expression MHC class I, class II or costsimulatory molecules CD80/86. However, infected DC were impaired in antigen presentation. PRRSV appears to suppress DC function.
Clinical signs and cellular and humoral immune responses were examined at MN in gilts challenged with heterologous or homologous strains 120 days after primary infection. No clinical signs were observed following homologous challenge. Mild clinical signs of fever, anorexia, and depression were observed in all heterologous challenge groups. Viremia was detected in all previously exposed groups challenged with all heterologous strains only on day 3 pi, and not at days 7 and 14 pi. Following homologous challenge, a vigorous CMI response and a weak humoral response were observed. Following heterologous challenge, weak or no CMI responses and vigorous humoral responses were observed.
Development of recombinant PRRSV vaccines using a herpes virus-based amplicon vector system containing the ORF 5 gene of PRRSV 23983 was performed by SD in collaboration with the U of Rochester. ORF 5 protein was detected by western blot using a PRRSV immune serum.
IL established a correlation between the two allelic forms of IL-12R?2 and the intensity of the interferon IFN-? response of swine to immunization with a PRRS MLV vaccine. The IL-12R?2 allele represents the first genetic marker in pigs associated with variation in the degree of cell-mediated immune response to a pig virus.
MO showed that viral growth on macrophages in the presence of interferon alpha was reduced in a manner dependent of viral isolate. PRRSV also suppressed IFN production in response to infection with TGEV, PRCV, polyI:C and VSV, all known IFN inducers. These results demonstrate that PRRSV field isolates differ both in IFN alpha sensitivity and induction. Furthermore, PRRSV field isolates differ in suppression of IFN induction by other viruses and double-stranded RNA.
IA identified anti-PRRSV antibody responses that were enhancing, neutralizing and neither. Identification of the epitopes responsible for enhancement or neutralization may provide the basis for developing efficacious second-generation vaccines. Serological characterization of auto-anti-idiotypic antibodies indicated that the Aab-2s recognized a site within or near the antigen-combining sites of the anti-GP5 antibodies. Aab-2 antibodies may play a role in immunity to PRRSV infection.
4. Develop improved methods for the diagnosis of PRRSV clinical disease and detection of virus and/or antibodies in PRRSV.
Real-time rapid PCR detection of PRRSV and vaccine in serum and semen was evaluated at KA and MO. North American and European ORF7 were amplified using a single set of PCR primers and distinguished by distinct melting peaks. Thus, detection of PRRSV RNA in semen is possible. At MO Lelystad strain and US/European PRRSV field isolates were successfully amplified. Multiplex assays incorporating both PRRSV genotypes and SIV also were developed. SD and NE, with Tetracore, Inc., validated a real-time PCR with primers specific for U.S. or European-like PRRSV. 427 semen and serum samples showed 95% agreement with nested RT-PCR. IA developed a multiplex RT-PCR assay for PRRSV, SIV and PCV2 in nasal swabs and lung lavage.
VA and IA developed a heteroduplex mobility assay (HMA) for quickly identifying PRRSV isolates similar to vaccines. The HMA results also correlated well with the results of phylogenetic analyses and indicate that HMA could be used as a rapid and efficient method for large-scale screening of potential vaccine-like PRRSV field isolates.
SD and MN validated a monoclonal antibody-based blocking ELISA using sera from 686 individual animals of known PRRSV status. Agreement with IDEXX ELISA and IFA for detection of seroconversion was demonstrated. IA also showed that blocking ELISA against nucleocapsid is sensitive and specific. NE, MS and SD determined that antibodies could be raised to PRRSV in ducks and rabbits. An experimental infection of Rouen and Mallard ducks showed no evidence of infection.
NC and SD collaborated to evaluate antibody responses in mature swine following repeated exposure to a single isolate of PRRSv by IDEXX 2XR commercial ELISA. All animals developed solidly positive antibody responses initially on HerdChek ELISA, but not on the HerdChek2XR. ELISA antibody levels dropped substantially 4 months after initial seroconversion, even in the face of repeated injections with virulent SD 28983 PRRSV. All animals remained FFN antibody positive at the end of the study. Challenge of the multiply exposed seronegative animals with a heterologous strain of PRRSV resulted in marked anamnestic ELISA and SN antibody responses.
IA, SD, and KA investigated PRRS ELISA false positive reactors. Ninety seven of 12,000 animals in PRRS-negative swine herds tested as false-positive by IDEXX ELISA. They were evaluated on 3 alternate ELISA-based serologic assays (developed at ISU, SDSU, and KSU) and were negative on at least one test. No test was 100% reliable. Western blotting did not reveal the cause of false positives.
Infectious clones of PRRSV were produced by SD in collaboration with Dr. Dongwan Yoo at Guelph University, Ontario, Canada and also shared with KA. A full-length clone of SD23983 containing a consensus 5end based on Genbank sequences of North American PRRSV strains is currently being tested. The infectious clone of VR2332 reported by Neilsen et al. was generously provided to SD and MO by MN. At MO, two rescue attempts with the VR-2332 clone both resulted in successful recovery of fully infectious virus with cytopathic effect and positive fluorescent-antibody staining indistinguishable from that of other PRRSV isolates. An infectious clone of PRRSV was constructed by NE from a highly abortifacient strain.
New 184 field isolates at MN have regions of radical dissimilarity all through the genome. SD and MN characterized European-like PRRSV isolates identified in the U.S. SD and KA focused on heterogeneity in the Nsp2 gene and a preliminary evaluation of phylogeny of these isolates. The ORF 1 of a European-like PRRSV isolate, SD 01-08, is organized the same as LV. The principal difference was a 17 aa deletion in Nsp2 of SD 01-08 that is not consistently observed. Evolutionary relationships among the European, North American and European-like isolates showed evidence for nucleotide diversity, including several deletions in the Nsp2 region. The European-like PRRSV isolates in the U.S. appear to be from a single Lelystad-like isolate.
KA and SD determined that the ratio of 2b to N in virion preparations was estimated to be approximately 20 N protein molecules for each 2b molecule. Thus 2b is a minor component of the PRRSV virion. KA and Guelph University determined that a single nuclear localization signal (NLS) is involved in the transport of N from the cytoplasm and into nucleus.
VA and IA collaborated on molecular analyses and biological characterizations of PRRSV field reisolates of vaccine and determined that the vaccine-like isolate 98-38803 induces microscopic pneumonia lesions similar in type to, but different in severity and time of onset from, those observed with virulent strains VR2385 and the parent strain of the vaccine.
Quasispecies diversity was analyzed in PRRSV in tonsils from 2 chronically infected farms in IL. All animals in the study harbored multiple, distinct PRRSV variants at both the nucleic acid and amino acid levels. The results indicate that PRRSV exists during natural infection as quasispecies distributions of related genotypes, but that positive natural selection for immune evasiveness in ORF5 does not appear to contribute to maintaining this diversity.
NE and IA conducted studies that indicated genetic variation in susceptibility to PRRSV. Future research with tissues collected will determine which genes are expressed differently in pigs with resistant and susceptible responses to PRRSV.
2. Determine the mechanism(s) and consequences of viral persistence.
NC developed and tested a serologic monitoring method to estimate the point-in-time portion of animals that are resistant to PRRSV, the portion that are susceptible, and the portion of animals that are infective. SD and MN examined the role of lymphoid and non-lymphoid tissue in acute and persistent infections of PRRSV. PRRSV disseminated to most tissues and lymph nodes in 2 d and was detected out to 70 dpi in various tissues. Lymphoid tissues play a prominent role as primary and persistent sites for PRRS viral replication.
MN detected PRRSV in flies in baited jug traps up to 1.66 km from an experimentally infected herd. Hence, transmission and persisttence of PRRSV in swine herds appears to involve flies and mosquitoes. Transport vehicles were also shown to effectively transmit PRRSV, but washing, disinfecting and drying eliminated PRRSV. Drying appeared to be an important component of a transport vehicle sanitation program for PRRSV biosecurity. Aerosolized PRRSV was transported 150 meters in a straight tube model and was infectious to susceptible pigs (MN). Attempts to infect mallard ducks with PRRSV via direct inoculation were not successful.
3. To characterize the different components of the immune response during acute and persistent infection and its implications in diagnostics and pathogenesis.
KA determined that the thymus is the principal site of virus replication in the fetus. IFN gamma and TNF were induced in lung and lymph nodes. IL and USDA-BARC reported an IFN gamma response to PRRSV after 5 weeks. A significant up-regulation of TNF indicated the involvement of innate immunity to PRRSV starting early in the infection, yet there was limited up-regulation of IFN alpha. Co-administration of IFN alpha caused faster returns to pre-vaccination levels for IL-6, IL-8 and IL-10 after 4 weeks. Co-administration of IFN alpha enhanced the IFN gamma response to vaccine. NE and IA produced chimeric mouse X pig anti-PRRSV antibodies that reacted with GP5 in ELISA and Western blot.
MN, NC, and IA collaborated to examine humoral immune responses to structural and nonstructural (nsp) proteins. PRRSV nsp 1, 2, and 4 were cloned. Direct ELISA to nsp 1 revealed that peak levels of antibody exceed anti-PRRSV nucleocapsid (N), and the levels were maintained for at least 120 days. Antibodies to nsp 4 appeared at low levels for a short time.
MN and IA collaborated to report that PRRSV-specific T cell responses were transient and varied substantially among animals. Viral loads decreased 1,000-fold in persistent infections, with tonsil being the primary site of persistence. A weak CMI response appears to contribute to prolonged PRRSV infection and suggests that PRRSV suppresses T cell recognition of infected macrophages. IL monitored the kinetics of the PRRSV-specific IFN gamma response in PBMC for 9 months. A weak IFN gamma response within a few weeks after vaccination appeared to wane at 10 weeks, then rebounded and, with fluctuation, increased gradually in intensity after a period of months without a booster immunization.
IL and NE exposed replacement gilts to a wild-type virus or a heterologous commercial vaccine. A higher IFN gamma response was associated with a lower proportion of stillborn pigs per litter. There was no relationship between humoral or cellular immune response and the recovery of PRRSV from the tonsil. ELISA antibodies were not predictive of any production variables. The use of a heterologous killed PRRS virus vaccine, following exposure to live virus, significantly boosted the cell-mediated immune response.
The role of dendritic cells (DC) in PRRSV pathogenesis and persistence was studied by SD and MN. PRRSV grew in pig DC and reduced expression of MHC class I, CD14, CD11b/c, but not MHC II. MN found no change of expression MHC class I, class II or costsimulatory molecules CD80/86. However, infected DC were impaired in antigen presentation. PRRSV appears to suppress DC function.
Clinical signs and cellular and humoral immune responses were examined at MN in gilts challenged with heterologous or homologous strains 120 days after primary infection. No clinical signs were observed following homologous challenge. Mild clinical signs of fever, anorexia, and depression were observed in all heterologous challenge groups. Viremia was detected in all previously exposed groups challenged with all heterologous strains only on day 3 pi, and not at days 7 and 14 pi. Following homologous challenge, a vigorous CMI response and a weak humoral response were observed. Following heterologous challenge, weak or no CMI responses and vigorous humoral responses were observed.
Development of recombinant PRRSV vaccines using a herpes virus-based amplicon vector system containing the ORF 5 gene of PRRSV 23983 was performed by SD in collaboration with the U of Rochester. ORF 5 protein was detected by western blot using a PRRSV immune serum.
IL established a correlation between the two allelic forms of IL-12R?2 and the intensity of the interferon IFN-? response of swine to immunization with a PRRS MLV vaccine. The IL-12R?2 allele represents the first genetic marker in pigs associated with variation in the degree of cell-mediated immune response to a pig virus.
MO showed that viral growth on macrophages in the presence of interferon alpha was reduced in a manner dependent of viral isolate. PRRSV also suppressed IFN production in response to infection with TGEV, PRCV, polyI:C and VSV, all known IFN inducers. These results demonstrate that PRRSV field isolates differ both in IFN alpha sensitivity and induction. Furthermore, PRRSV field isolates differ in suppression of IFN induction by other viruses and double-stranded RNA.
IA identified anti-PRRSV antibody responses that were enhancing, neutralizing and neither. Identification of the epitopes responsible for enhancement or neutralization may provide the basis for developing efficacious second-generation vaccines. Serological characterization of auto-anti-idiotypic antibodies indicated that the Aab-2s recognized a site within or near the antigen-combining sites of the anti-GP5 antibodies. Aab-2 antibodies may play a role in immunity to PRRSV infection.
4. Develop improved methods for the diagnosis of PRRSV clinical disease and detection of virus and/or antibodies in PRRSV.
Real-time rapid PCR detection of PRRSV and vaccine in serum and semen was evaluated at KA and MO. North American and European ORF7 were amplified using a single set of PCR primers and distinguished by distinct melting peaks. Thus, detection of PRRSV RNA in semen is possible. At MO Lelystad strain and US/European PRRSV field isolates were successfully amplified. Multiplex assays incorporating both PRRSV genotypes and SIV also were developed. SD and NE, with Tetracore, Inc., validated a real-time PCR with primers specific for U.S. or European-like PRRSV. 427 semen and serum samples showed 95% agreement with nested RT-PCR. IA developed a multiplex RT-PCR assay for PRRSV, SIV and PCV2 in nasal swabs and lung lavage.
VA and IA developed a heteroduplex mobility assay (HMA) for quickly identifying PRRSV isolates similar to vaccines. The HMA results also correlated well with the results of phylogenetic analyses and indicate that HMA could be used as a rapid and efficient method for large-scale screening of potential vaccine-like PRRSV field isolates.
SD and MN validated a monoclonal antibody-based blocking ELISA using sera from 686 individual animals of known PRRSV status. Agreement with IDEXX ELISA and IFA for detection of seroconversion was demonstrated. IA also showed that blocking ELISA against nucleocapsid is sensitive and specific. NE, MS and SD determined that antibodies could be raised to PRRSV in ducks and rabbits. An experimental infection of Rouen and Mallard ducks showed no evidence of infection.
NC and SD collaborated to evaluate antibody responses in mature swine following repeated exposure to a single isolate of PRRSv by IDEXX 2XR commercial ELISA. All animals developed solidly positive antibody responses initially on HerdChek ELISA, but not on the HerdChek2XR. ELISA antibody levels dropped substantially 4 months after initial seroconversion, even in the face of repeated injections with virulent SD 28983 PRRSV. All animals remained FFN antibody positive at the end of the study. Challenge of the multiply exposed seronegative animals with a heterologous strain of PRRSV resulted in marked anamnestic ELISA and SN antibody responses.
IA, SD, and KA investigated PRRS ELISA false positive reactors. Ninety seven of 12,000 animals in PRRS-negative swine herds tested as false-positive by IDEXX ELISA. They were evaluated on 3 alternate ELISA-based serologic assays (developed at ISU, SDSU, and KSU) and were negative on at least one test. No test was 100% reliable. Western blotting did not reveal the cause of false positives.
Impacts
- Full-length infectious clones of virulent and attenuated PRRSV strains of North American and European genotypes will be powerful tools for elucidation of the genetic similarities and differences in PRRSV isolates that control phenotypic variation in pathogenesis and immune sensitivity as well as assist the development of a genetically-engineered marker vaccine of PRRSV.
- Understanding the genetic basis for host susceptibility to disease, and the role of concurrent infections in pathogenesis will help to develop disease resistant pigs based on genetically desirable traits.
- Information of the various routes of PRRSV transmission is essential to protect commercial swine operation from becoming infected.
- Knowing that lymphoid tissues play a prominent role as both primary and persistent sites for PRRS viral replication will improve studies of disease pathogenesis and immune protection.
- PRRSV Nsp2 may be useful as a marker for diversity within the group of European-like and North American PRRSV isolates.
- Understanding the mechanisms that regulate the development of anti-viral protective immunity will lead to the development of more effective vaccines and adjuvants, and assist in developing better methods to monitor immunity.
- Knowledge of viral mechanisms of immunosuppression, especially suppression of the innate immune response, will help elucidate improve methods of PRRSV control through vaccination.
- Studies with dendritic cells will provide insight into the mechanisms for viral persistence and immune modulation associated with PRRSV, while new vaccine strategies may eventually offer improved methods for the control of PRRS.
- Application of real-time, quantitative PCR assay has broad potential for commercial use in boar studs, diagnostic laboratories and other facilities for monitoring PRRSV infection and biosecurity for the detection of U.S and Lelystad or European-like PRRSV.
- The blocking ELISA offers an alternative to the IFA for follow-up of suspect PRRS serological results.
- The use of cell culture adapted European-like PRRSV isolates of U.S. origin in routine diagnostic IFA and virus neutralization assays allows for improved serological monitoring without the restrictions associated with imported European isolates, such as LV.
Publications
Bastos, R.G., O.A. Dellagostin, R.G. Barletta, A.R. Doster, E.A. Nelson and F.A. Osorio. 2002. Construction and immumogenicity of recombinant Mycobacterium bovis BCG expressing GP5 and M protein of porcine reproductive and respiratory syndrome virus. Vaccine 21:21-29.
Batista L, Dee S, Molitor T, Olin M, Joo HS, Pijoan C, Murtaugh MP, Xiao Z, Rossow K, Polson D. 2004. Detection of porcine reproductive and respiratory syndrome virus in pigs with low positive or negative ELISA sample-to-positive ratios. Vet Rec. 154:25-26.
Batista L, Lwamba H, Pijoan C, Johnson CR, Murtaugh MP. 2004. Genetic diversity of porcine reproductive and respiratory syndrome virus (PRRSV) in two regions of Mexico. In press.
Cafruny, WA, QA Jones, TR Haven, NL Zitterkopf, PGW Plagemann and RRR Rowland. 2003. Glucocorticoid regulation of lactate dehydrogenase-elevating virus replication in macrophages, Virus Res, 92:83-87.
Cancel-Tirado SM, Yoon K-J. 2003. Antibody dependent enhancement of virus infection and disease. Viral Immunol 16:69-86
Dee SA, Deen J, Pijoan C. 2004. An evaluation of four intervention strategies to prevent mechanical transmission of porcine reproductive and respiratory syndrome virus. Can J Vet Res In press.
Dee SA, Deen J, Rossow KD, Eliason R, Mahlum C, Otake S, Joo HS, and Pijoan C. 2003. Mechanical transmission of porcine reproductive and respiratory syndrome virus throughout a coordinated sequence of events during warm weather. Can J Vet Res 67:12-16.
Dee SA. 2003. Approaches to prevention, control and eradication of PRRS. National Pork Board PRRS Compendium, 2nd edition, 119-130.
Feng, W-H, Laster, SM, Tompkins, M, Brown, TT, Xu, J-S, Gomez, W, Benfield, D, and McCaw, MB. 2002. Thymocyte and peripheral blood T lymphocyte subpopulation changes in piglets following in utero infection with porcine reproductive and respiratory syndrome virus. Virology 302:363-372.
Feng, W-H, Tompkins, M. Xu, J., Zhang, H-X., McCaw, MB. 2003. Analysis of constitutive cytokine expression by pigs infected in-utero with porcine reproductive and respiratory syndrome virus. Vet Immuno Immunopath. 94:35-45.
Ferrin, N.H., Y. Fang, C.R. Johnson, M.P. Murtaugh, D.D. Polson and E.A. Nelson. 2004. Validation of a blocking ELISA for the detection of antibodies against porcine reproductive and respiratory syndrome virus. Clinical and Diagnostic Laboratory Immunology. In press.
Foss, D.L., M.J. Zilliox, W. Meier, F. Zuckermann, and M.P. Murtaugh. 2002. Adjuvant danger signals increase the immune response to porcine reproductive and respiratory syndrome virus. Viral Immunol. 15:557-566.
Goldberg, T. L., J. F. Lowe, S. M. Milburn, L. D. Firkins. 2004. Quasispecies diversity of porcine reproductive and respiratory syndrome virus during natural infection. Virology. 317:197-207.
Hermann JR, Honeyman MS, Zimmerman JJ, Thacker BJ, Holden PJ, Chang CC. 2003. Effect of dietary Echinacea purpurea on viremia and performance in porcine reproductive and respiratory syndrome virus-infected nursery pigs. J An Sci 81:2139-2144.
Jiang Z, Zhou E-M, Ameri-Hahabadi M, Zimmerman JJ, Platt KB. 2003. Identification and characterization of auto-anti-idiotypic antibodies specific for antibodies against porcine reproductive and respiratory syndrome virus envelope glycoprotein (GP5). Vet Immunol Immunopathol 92:125-135.
Key K, Guenette DK, Yoon K-J, Halbur PG, Toth TE, Meng X-J. 2003. Identification and differentiation of vaccine-like isolates of porcine reproductive and respiratory syndrome virus from field isolates using a heteroduplex mobility assay. J Clin Microbiol 41:2433-2439
Kleiboeker, S.B., Lehman, J.R., and Fangman, T.J. 2002. Concurrent use of reverse transcription-polymerase chain reaction testing of oropharyngeal scrapings and paired serological testing for detection of porcine reproductive and respiratory syndrome virus in sows. J Swine Health Production 10:251-258.
Meier WA, Judy Galeota J, Osorio FA, Husmann R, Schnitzlein W, and Zuckermann FA. 2003. Gradual Development of the Interferon__ Response of Swine to Porcine Reproductive and Respiratory Syndrome Virus. Virol. 309:18-31
Murtaugh, M.P. Z. Xiao, and F. Zuckermann. 2002. Immunological responses of swine to porcine reproductive and respiratory syndrome virus infection. Viral Immunol. 15:533-547.
Murtaugh, M.P., Z. Xiao, M.S. Rutherford and F. Zuckermann. 2003. Immunology. The PRRS (Porcine Arterivirus) Compendium (2nd Edition). Section 5.3. 28 pp. National Pork Board, Clive, Iowa.
Nielsen, H.S., Liu, G.-P., Nielsen, J., Oleksiewicz, M. B., Bxtner, A., Storgaard, T. and K.S. Faaberg. 2003. Generation of an infectious clone of VR-2332, a highly virulent North American-type isolate of porcine reproductive and respiratory syndrome virus. J. Virol., 77:3702-3711.
Opriessnig T, Halbur PG, Yoon K-J, Pogranichniy RM, Harmon KM, Evans R, Key KF, Pallares FJ, Thomas P, Meng X-J. 2002. Comparison of molecular and biological characteristics of a modified live PRRSV vaccine (Ingelvac PRRS MLV), the parent strain of the vaccine (ATCC VR2332), ATCC VR2385, and two recent field isolates of PRRSV. J Virol 76:11837-11844.
Osorio, F.A., J.A. Galeota, E.A. Nelson, B. Broderson, A. Doster, R. Wills, F. Zuckermann and W.W. Laegreid. 2002. Passive transfer of virus-specific neutralizing antibodies confers protection against reproductive failure induced by a virulent strain of porcine reproductive and respiratory syndrome virus and establishes sterilizing immunity. Virology, 302:9-20.
Otake S, Dee SA, Moon RD, Rossow KD, Trincado C and Pijoan C. 2003. Evaluation of mosquitoes, Aedes vexans, as biological vectors of porcine reproductive and respiratory syndrome virus. Can J Vet Res 67:265-270.
Otake S, Dee SA, Moon RD, Rossow KD, Trincado C, and Pijoan C. 2003. Transmission of porcine reproductive and respiratory syndrome virus by houseflies (Musca domestica). Vet Rec 152:73-76.
Otake S, Dee SA, Moon RD, Rossow KD, Trincado C, Farnham M, and Pijoan C. 2003. Survival of porcine reproductive and respiratory syndrome virus in houseflies . Can J Vet Res 67:198-203.
Reilly, C., C. Wang, and M.S. Rutherford, 2003. A method for the normalizing microarrays using the genes that are not differentially expressed. J. Amer. Statistical Assoc., in press.
Ropp, S. L., Mahlum Wees, C. E., Fang, Y., Nelson, E. A., Rossow, K. D., Bien, M., Arndt, B., Preszler, S., Steen, P., Christopher-Hennings, J., Collins, J. E., Benfield, D. A., and K. S. Faaberg 2003. Characterization of emerging European-like PRRSV isolates in the United States. J. Virol., accepted for publication.
Rowland, R.R.R., S. Lawson, K. Rossow and D. Benfield. 2003. Lymphoid tissue tropism of porcine reproductive and respiratory syndrome virus replication during persistent infection of pigs originally exposed to virus in utero. Vet Microbiol. 96:219-235.
Rowland, RRR and D Yoo. 2003. Nucleolar-cytoplasmic shuttling of the PRRSV nucleocapsid protein: a simple case of molecular mimicry or the complex regulation by nuclear import, nucleolar localization and nuclear export signal sequences. Virus Res, 95:23-33.
Rowland, RRR, P Schneider, Y Fang, S Wootton, D Yoo, and DA Benfield. 2003. Peptide domains involved in the localization of the porcine reproductive and respiratory syndrome virus nucleocapsid protein to the nucleolus. Virology 316:135-145.
Thanawongnuwech, R., Young, T.F., Thacker, B.J., Halbur, P.G., Thacker, E.L. 2003. Interleukin (IL) 10, IL 12, and interferon gamma levels in the respiratory tract following Mycoplasma hyopneumoniae and PRRS infection in pigs. Viral Immunol., 16:357-367,
Wills R.W., Doster AR, Galeota JA, Sur JH, Osorio FA. 2003. Duration of infection and proportion of pigspersistently infected with porcine reproductive and respiratory syndrome virus (PRRSV). J Clin Micro 41:58-62.
Xiao Z, Batista L, Dee S, Halbur P, Murtaugh MP. 2004. The level of virus-specific T-cell and macrophage recruitment in porcine reproductive and respiratory syndrome virus infection in pigs is independent of the virus load. J. Virol. In press.
Yoo D, SK Wootton, G Li, C Song and RRR Rowland. 2003. Colocalization and interaction of the porcine arterivirus nucleocapsid protein with the small nucleolar RNA-associated protein fibrillarin. J. Virol. 77:12173-12183.
Yoon K-J, Christopher-Hennings J, Nelson E. 2003. Diagnosis of PRRS. In: J.J. Zimmerman, K.-J. Yoon and E. Neumann (eds). 2003 PRRS Compendium: A reference for pork producers, pp. 55-67. National Pork Board, Des Moines, Iowa.
Yoon K-J, Christopher-Hennings J, Nelson E. 2003. Diagnosis. In: J.J. Zimmerman JJ and K.-J. Yoon (eds). 2003 PRRS Compendium: A comprehensive reference on PRRS for pork producers, veterinary practitioners, and researchers (2nd edition), pp 59-74. National Pork Board, Des Moines, Iowa.
Yoon K-J, Stevenson G. 2002. Porcine reproductive and respiratory syndrome: Diagnosis. In: A. Morilla, K.-J. Yoon and J.J. Zimmerman (eds). Trends in emerging viral infections of swine, pp 347-354. Iowa State University Press, Ames, Iowa
Yoon K-J. 2002. Porcine reproductive and respiratory syndrome: Virology. In: A. Morilla, K.-J. Yoon and J.J. Zimmerman (eds). Trends in emerging viral infections of swine, pp 339-346. Iowa State University Press, Ames, Iowa
Yoon K-J. 2003. Virology. In: J.J. Zimmerman JJ and K.-J. Yoon (eds). 2003 PRRS Compendium: A comprehensive reference on PRRS for pork producers, veterinary practitioners, and researchers (2nd edition), pp 163-184. National Pork Board, Des Moines, Iowa.
Yuan S, Murtaugh MP, Schumann FA, Mickelson D, and Faaberg KS. 2003. Characterization of heteroclite subgenomic RNAs associated with PRRSV infection. Virology. In press.
Zhou E-M, Jiang Z, Ameri-Mahabadi M, Zimmerman JJ. 2003. Detection and characterization of auto-anti-idiotypic antibodies specific for Idiotypic antibodies against envelope glycoprotein and matrix protein of porcine reproductive and respiratory syndrome virus. J Virol Methods (in press).
Zimmerman J. Epidemiology and ecology. 2003. In: The Porcine Reproductive and Respiratory Syndrome Compendium: A comprehensive reference on PRRS for pork producers, veterinary practitioners, and researchers (2nd edition). Zimmerman JJ, Yoon K-J (eds). National Pork Board, Des Moines Iowa, pp.27-50.
Zimmerman J. Historical overview. 2003. In: The Porcine Reproductive and Respiratory Syndrome Compendium: A comprehensive reference on PRRS for pork producers, veterinary practitioners, and researchers (2nd edition). Zimmerman JJ, Yoon K-J (eds). National Pork Board, Des Moines Iowa, pp.1-6.
Zimmerman JJ, Yoon K-J (editors). 2003. PRRS Compendium: A comprehensive reference on PRRS for pork producers, veterinary practitioners, and researchers (2nd edition). National Pork Board, Des Moines, Iowa. 294 pages
PROCEEDINGS AND ABSTRACTS:
Callahan, J.D., J. Christopher-Hennings, T.A. Gay, M.E. Reos, Y.Fang, M. Dammen, A. Wasilk, J. Galeota, F.A. Osorio, M. Torremorell, W.M. Nelson and E.A. Nelson. 2003. Development, validation and commercialization of a real-time RT-PCR assay for the detection of Lelystad, European-like and US Porcine reproductive and respiratory syndrome viruses. 107th Annual Meeting of the American Assoc. of Vet. Lab. Diagnostitions, p. 142.
Carlson, D.L., A.N. Wasilk, Y. Fang, S.A.E. Marras, E.A. Nelson and J. Christopher-Hennings. 2002. Detection, differentiation and quantitation of PRRSV strains by real-time RT-PCR with molecular beacons. 83rd Conf. of Research Workers in Animal Disease.
Christopher-Hennings, J., J. Callahan, T. Gay, A. Wasilk, Y. Fang, M. Dammen, M. Torremorell, D. Polson, M. Mellencamp, E.A. Nelson and W.M. Nelson. 2003. Validation of a real-time, quantitative PCR assay to detect U.S. and Lelystad/European-like PRRSV in boar semen and serum. 84th Conf. of Research Workers in Animal Disease.
Faaberg KS, Murtaugh MP, Mahlum-Wees CE, Johnson JE, Dwan C. 2003. Evolution of ORF5 in North America over 15 years. Proc. IXth International Symposium of Nidoviruses. 4.4, Egmond aan Zee, The Netherlands.
Faaberg, K. S., Murtaugh, M. P., Mahlum-Wees, C. E., Johnson, J. E., and C. Dwan. 2003. PRRSV: Evolution of ORF5 in North America over 15 years. IXth International Symposium on Nidoviruses,
Fang, Y., D. Kim, R.R.R. Rowland, S. Ropp, P. Steen, J. Christopher-Hennings and E.A. Nelson. 2003. Heterogeneity in the NSP2 gene of European-like PRRSV isolated in the United States. 84th Conf. of Research Workers in Animal Disease.
Fang, Y., W.P. Zhang, R.R.R. Rowland, J. Christopher-Hennings and E.A. Nelson. 2003. Phylogeny of European-like PRRSV isolates in North America. 84th Conf. of Research Workers in Animal Disease.
Ferrin, N.H., Y. Fang, D.D. Polson, M. Torremorell, M. Gramer, M.P. Murtaugh, C.R. Johnson, and E.A. Nelson. 2002. Validation of a blocking ELISA for antibodies against PRRSV. 83rd Conf. of Research Workers in Animal Disease.
Goldberg, T. L., J. F. Lowe, S. M. Milburn, L. D. Firkins. 2003. Quasispecies diversity of porcine reproductive and respiratory syndrome virus during natural infection. CRWAD 2003 Proceedings. ISU Press. Abst 153.
Hadley, L., Xu, J-S., McCaw, M.B., and Laster, S. 2002. Purified proteins from an acute strain of PRRSv provide protection via TH1-type immune response. In: Proceedings of 17th Congress of the International Pig Veterinary Society, Ames, Iowa, USA.
Liu, G., Nielsen, H. S., Burkhart, K. M., Roof, M. B., Vaughn, E. M., and K. S. Faaberg. 2003. Porcine Respiratory and Reproductive Syndrome Virus (PRRSV) Infectious Clones Reveal Nucleotides Important for Genome Replication. IXth International Symposium on Nidoviruses, P.6.6, Egmond aan Zee, The Netherlands.
Liu, G., Nielsen, H. S., Zhiming, O., and K. S. Faaberg. 2003. Infectivity of porcine respiratory syndrome virus genomic clones. 21th Annual Meeting of the American Society for Virology, W14-5, Davis, CA.
Lowe J.F., L.D. Firkins, F. A. Zuckerman, T.L. Goldberg. 2003. Immune response and reproductive performance in swine following known infection with PRRS virus in commercial herds. CRWAD 2003 Proceedings. ISU Press. Abst 144.
McCaw, M.B. Roberts, J, Laster, S.M., Hadley, L., and Erickson, G.A. 2003. Characterization of PRRSv antibody and rtPCR responses following repeated exposures and then challenge with homologous wild-type virus. In: Proceedings of 4th International Symposium on Emerging and Re-emerging Pig Diseases, Rome, Italy. pp 81-82.
McCaw, M.B., J. Roberts, J.J. Zimmerman, Laster, S., Hadley, L.,G.A. Erickson. 2002. PRRSv ELISA response and PCR viremia following repeated homologous exposures to wild-type virus in adult swine. Conference in Research Workers in Animal Disease. St. Louis, MO.
McCaw, M.B., Roberts, J., Laster, S., Hadley, L., and Erickson, G.A. 2002. PRRSv serologic assay limitations following repeated homologous exposures to wild-type virus in adult swine. In: Proceedings of 17th Congress of the International Pig Veterinary Society, 2002, Ames, Iowa, USA. p208.
Mondaca-Fernandez E, Morrison RB, Murtaugh MP. 2003. Using GIS and sequencing to assess regional epidemiology of PRRSV. Proc. Allen D. Leman Swine Conf. 30:71-74.
Murtaugh MP, Harding J, Faaberg KS. 2003. Genetic variation and biological safety of Ingelvac MLV modified live PRRS vaccine during seven years of continuous use in the field. 4th International Symposium on Emerging and Re-emerging Pig Diseases. Rome.
Murtaugh MP, Harding J. 2003. PRRS virus genomics: application to a field investigation. Proc. Allen D. Leman Swine Conf. 30:41-43.
Murtaugh MP, Wees CE, Johnson JE, Dwan C,Faaberg KS. 2003. Molecular evolution of porcine reproductive and respiratory syndrome virus (PRRSV) envelope glycoprotein 5. 4th International Symposium on Emerging and Re-emerging Pig Diseases. Abstract 57. Rome.
Murtaugh MP, Xiao Z, Johnson CR, Dee SA Batista L. 2003. Porcine immunity to porcine reproductive and respiratory syndrome virus (PRRSV): systemic and local responses in acute and persistent infection. Proc. IXth International Symposium of Nidoviruses
Petry DB, Holl JW, Weber J, Doster AR, Osorio FA, and RK Johnson. 2004. Different biological responses of pigs of two genetic populations to PRRSV challenge suggests underlying genetic variation in susceptibility/resistance to PRRSV, Nebraska Swine Report (In press)
Roof, M. B., Vaughn, E. M., Burkhart, K. M., and K.S. Faaberg. 2003. Efficacy of modified live virus porcine reproductive and respiratory virus vaccines against heterologous respiratory challenge. 4th International Symposium on Emerging and Re-emerging Pig Diseases: PRRS, PMWS, Swine Influenza. Abstract 15, 45-16, Rome, Italy.
Ropp, S.L., Y. Fang, M. Bien, B. Arndt, S. Preszler, P. Steen, J. Christopher-Hennings, D.A. Benfield and E. A. Nelson. 2002. Antigenic and genetic characterization of emerging European-like PRRSV isolates in the United States. 83rd Conf. of Research Workers in Animal Disease.
Royaee A, F.A. Zuckermann, R. Husmann, G. Calzada-Nova, W. Schnitzlein, J.K. Lunney. 2003. T cell cytokine response and gene expression profile of porcine lymphoid cells in response to vaccination with PRRS virus. CRWAD 2003 Proceedings. ISU Press. Abst. 115.
Thacker E, Kittikoon P, Vincent A, Hipple K, Nilubol D, Yu S, Janke B, Thacker B. 2003. Influence of PRRS virus infection on swine influenza vaccine efficacy. Emerging Disease Conference, Rome, Italy.
Vincent A, Thacker B, Halbur P, Rothschild M, Thacker E. 2003. An investigation of susceptibility to porcine reproductive and respiratory syndrome virus between genetically diverse lines of pigs. CRWAD, Chicago, Il Nov 10, 2003.
Waldner, D., D. Zeman, A. Kasuske, S. Ropp, B. Arndt, E. Nelson and D. Benfield. 2003. Lymphoid tissues may represent not only sites of persistence but early sites of replication of porcine reproductive and respiratory syndrome (PRRS) virus. 84th Conf. of Research Workers in Animal Disease.
Waldner, D., D. Zeman, A. Kasuske, S. Ropp, B. Arndt, E. Nelson, Y. Fang and D. Benfield. 2003. Temporal studies on the replication of PRRS virus in conventional pigs from six hours to 126 days post-inoculation. 107th Annual Meeting of the American Assoc. of Vet. Lab. Diagnostitions, p. 141.
Xiao Z, Murtaugh MP, Johnson CR, Batista L, Dee SA. 2003. Immunity to porcine reproductive and respiratory syndrome virus (PRRSV): systemic and local responses in acute and persistent infection. 4th International Symposium on Emerging and Re-emerging Pig Diseases. Rome.
Yoon KJ, Chang CC, Zimmerman JJ, Harmon KH, Dixon PH, Murtaugh MP. 2003. Molecular evolution of PRRSV during prolonged in vivo replication. 4th International Symposium on Emerging and Re-emerging Pig Diseases. Rome.
Zuckermann, F.A., Schnitzlein, W., Husmann, R., and Calzada-Nova, G. 2003. Association of porcine interleukin-12 receptor beta 2 (IL-12Rb2) gene alleles with the development of high or low interferon-? response to PRRS virus. CRWAD 2003 Proceedings. ISU Press. Abst 114.
Batista L, Dee S, Molitor T, Olin M, Joo HS, Pijoan C, Murtaugh MP, Xiao Z, Rossow K, Polson D. 2004. Detection of porcine reproductive and respiratory syndrome virus in pigs with low positive or negative ELISA sample-to-positive ratios. Vet Rec. 154:25-26.
Batista L, Lwamba H, Pijoan C, Johnson CR, Murtaugh MP. 2004. Genetic diversity of porcine reproductive and respiratory syndrome virus (PRRSV) in two regions of Mexico. In press.
Cafruny, WA, QA Jones, TR Haven, NL Zitterkopf, PGW Plagemann and RRR Rowland. 2003. Glucocorticoid regulation of lactate dehydrogenase-elevating virus replication in macrophages, Virus Res, 92:83-87.
Cancel-Tirado SM, Yoon K-J. 2003. Antibody dependent enhancement of virus infection and disease. Viral Immunol 16:69-86
Dee SA, Deen J, Pijoan C. 2004. An evaluation of four intervention strategies to prevent mechanical transmission of porcine reproductive and respiratory syndrome virus. Can J Vet Res In press.
Dee SA, Deen J, Rossow KD, Eliason R, Mahlum C, Otake S, Joo HS, and Pijoan C. 2003. Mechanical transmission of porcine reproductive and respiratory syndrome virus throughout a coordinated sequence of events during warm weather. Can J Vet Res 67:12-16.
Dee SA. 2003. Approaches to prevention, control and eradication of PRRS. National Pork Board PRRS Compendium, 2nd edition, 119-130.
Feng, W-H, Laster, SM, Tompkins, M, Brown, TT, Xu, J-S, Gomez, W, Benfield, D, and McCaw, MB. 2002. Thymocyte and peripheral blood T lymphocyte subpopulation changes in piglets following in utero infection with porcine reproductive and respiratory syndrome virus. Virology 302:363-372.
Feng, W-H, Tompkins, M. Xu, J., Zhang, H-X., McCaw, MB. 2003. Analysis of constitutive cytokine expression by pigs infected in-utero with porcine reproductive and respiratory syndrome virus. Vet Immuno Immunopath. 94:35-45.
Ferrin, N.H., Y. Fang, C.R. Johnson, M.P. Murtaugh, D.D. Polson and E.A. Nelson. 2004. Validation of a blocking ELISA for the detection of antibodies against porcine reproductive and respiratory syndrome virus. Clinical and Diagnostic Laboratory Immunology. In press.
Foss, D.L., M.J. Zilliox, W. Meier, F. Zuckermann, and M.P. Murtaugh. 2002. Adjuvant danger signals increase the immune response to porcine reproductive and respiratory syndrome virus. Viral Immunol. 15:557-566.
Goldberg, T. L., J. F. Lowe, S. M. Milburn, L. D. Firkins. 2004. Quasispecies diversity of porcine reproductive and respiratory syndrome virus during natural infection. Virology. 317:197-207.
Hermann JR, Honeyman MS, Zimmerman JJ, Thacker BJ, Holden PJ, Chang CC. 2003. Effect of dietary Echinacea purpurea on viremia and performance in porcine reproductive and respiratory syndrome virus-infected nursery pigs. J An Sci 81:2139-2144.
Jiang Z, Zhou E-M, Ameri-Hahabadi M, Zimmerman JJ, Platt KB. 2003. Identification and characterization of auto-anti-idiotypic antibodies specific for antibodies against porcine reproductive and respiratory syndrome virus envelope glycoprotein (GP5). Vet Immunol Immunopathol 92:125-135.
Key K, Guenette DK, Yoon K-J, Halbur PG, Toth TE, Meng X-J. 2003. Identification and differentiation of vaccine-like isolates of porcine reproductive and respiratory syndrome virus from field isolates using a heteroduplex mobility assay. J Clin Microbiol 41:2433-2439
Kleiboeker, S.B., Lehman, J.R., and Fangman, T.J. 2002. Concurrent use of reverse transcription-polymerase chain reaction testing of oropharyngeal scrapings and paired serological testing for detection of porcine reproductive and respiratory syndrome virus in sows. J Swine Health Production 10:251-258.
Meier WA, Judy Galeota J, Osorio FA, Husmann R, Schnitzlein W, and Zuckermann FA. 2003. Gradual Development of the Interferon__ Response of Swine to Porcine Reproductive and Respiratory Syndrome Virus. Virol. 309:18-31
Murtaugh, M.P. Z. Xiao, and F. Zuckermann. 2002. Immunological responses of swine to porcine reproductive and respiratory syndrome virus infection. Viral Immunol. 15:533-547.
Murtaugh, M.P., Z. Xiao, M.S. Rutherford and F. Zuckermann. 2003. Immunology. The PRRS (Porcine Arterivirus) Compendium (2nd Edition). Section 5.3. 28 pp. National Pork Board, Clive, Iowa.
Nielsen, H.S., Liu, G.-P., Nielsen, J., Oleksiewicz, M. B., Bxtner, A., Storgaard, T. and K.S. Faaberg. 2003. Generation of an infectious clone of VR-2332, a highly virulent North American-type isolate of porcine reproductive and respiratory syndrome virus. J. Virol., 77:3702-3711.
Opriessnig T, Halbur PG, Yoon K-J, Pogranichniy RM, Harmon KM, Evans R, Key KF, Pallares FJ, Thomas P, Meng X-J. 2002. Comparison of molecular and biological characteristics of a modified live PRRSV vaccine (Ingelvac PRRS MLV), the parent strain of the vaccine (ATCC VR2332), ATCC VR2385, and two recent field isolates of PRRSV. J Virol 76:11837-11844.
Osorio, F.A., J.A. Galeota, E.A. Nelson, B. Broderson, A. Doster, R. Wills, F. Zuckermann and W.W. Laegreid. 2002. Passive transfer of virus-specific neutralizing antibodies confers protection against reproductive failure induced by a virulent strain of porcine reproductive and respiratory syndrome virus and establishes sterilizing immunity. Virology, 302:9-20.
Otake S, Dee SA, Moon RD, Rossow KD, Trincado C and Pijoan C. 2003. Evaluation of mosquitoes, Aedes vexans, as biological vectors of porcine reproductive and respiratory syndrome virus. Can J Vet Res 67:265-270.
Otake S, Dee SA, Moon RD, Rossow KD, Trincado C, and Pijoan C. 2003. Transmission of porcine reproductive and respiratory syndrome virus by houseflies (Musca domestica). Vet Rec 152:73-76.
Otake S, Dee SA, Moon RD, Rossow KD, Trincado C, Farnham M, and Pijoan C. 2003. Survival of porcine reproductive and respiratory syndrome virus in houseflies . Can J Vet Res 67:198-203.
Reilly, C., C. Wang, and M.S. Rutherford, 2003. A method for the normalizing microarrays using the genes that are not differentially expressed. J. Amer. Statistical Assoc., in press.
Ropp, S. L., Mahlum Wees, C. E., Fang, Y., Nelson, E. A., Rossow, K. D., Bien, M., Arndt, B., Preszler, S., Steen, P., Christopher-Hennings, J., Collins, J. E., Benfield, D. A., and K. S. Faaberg 2003. Characterization of emerging European-like PRRSV isolates in the United States. J. Virol., accepted for publication.
Rowland, R.R.R., S. Lawson, K. Rossow and D. Benfield. 2003. Lymphoid tissue tropism of porcine reproductive and respiratory syndrome virus replication during persistent infection of pigs originally exposed to virus in utero. Vet Microbiol. 96:219-235.
Rowland, RRR and D Yoo. 2003. Nucleolar-cytoplasmic shuttling of the PRRSV nucleocapsid protein: a simple case of molecular mimicry or the complex regulation by nuclear import, nucleolar localization and nuclear export signal sequences. Virus Res, 95:23-33.
Rowland, RRR, P Schneider, Y Fang, S Wootton, D Yoo, and DA Benfield. 2003. Peptide domains involved in the localization of the porcine reproductive and respiratory syndrome virus nucleocapsid protein to the nucleolus. Virology 316:135-145.
Thanawongnuwech, R., Young, T.F., Thacker, B.J., Halbur, P.G., Thacker, E.L. 2003. Interleukin (IL) 10, IL 12, and interferon gamma levels in the respiratory tract following Mycoplasma hyopneumoniae and PRRS infection in pigs. Viral Immunol., 16:357-367,
Wills R.W., Doster AR, Galeota JA, Sur JH, Osorio FA. 2003. Duration of infection and proportion of pigspersistently infected with porcine reproductive and respiratory syndrome virus (PRRSV). J Clin Micro 41:58-62.
Xiao Z, Batista L, Dee S, Halbur P, Murtaugh MP. 2004. The level of virus-specific T-cell and macrophage recruitment in porcine reproductive and respiratory syndrome virus infection in pigs is independent of the virus load. J. Virol. In press.
Yoo D, SK Wootton, G Li, C Song and RRR Rowland. 2003. Colocalization and interaction of the porcine arterivirus nucleocapsid protein with the small nucleolar RNA-associated protein fibrillarin. J. Virol. 77:12173-12183.
Yoon K-J, Christopher-Hennings J, Nelson E. 2003. Diagnosis of PRRS. In: J.J. Zimmerman, K.-J. Yoon and E. Neumann (eds). 2003 PRRS Compendium: A reference for pork producers, pp. 55-67. National Pork Board, Des Moines, Iowa.
Yoon K-J, Christopher-Hennings J, Nelson E. 2003. Diagnosis. In: J.J. Zimmerman JJ and K.-J. Yoon (eds). 2003 PRRS Compendium: A comprehensive reference on PRRS for pork producers, veterinary practitioners, and researchers (2nd edition), pp 59-74. National Pork Board, Des Moines, Iowa.
Yoon K-J, Stevenson G. 2002. Porcine reproductive and respiratory syndrome: Diagnosis. In: A. Morilla, K.-J. Yoon and J.J. Zimmerman (eds). Trends in emerging viral infections of swine, pp 347-354. Iowa State University Press, Ames, Iowa
Yoon K-J. 2002. Porcine reproductive and respiratory syndrome: Virology. In: A. Morilla, K.-J. Yoon and J.J. Zimmerman (eds). Trends in emerging viral infections of swine, pp 339-346. Iowa State University Press, Ames, Iowa
Yoon K-J. 2003. Virology. In: J.J. Zimmerman JJ and K.-J. Yoon (eds). 2003 PRRS Compendium: A comprehensive reference on PRRS for pork producers, veterinary practitioners, and researchers (2nd edition), pp 163-184. National Pork Board, Des Moines, Iowa.
Yuan S, Murtaugh MP, Schumann FA, Mickelson D, and Faaberg KS. 2003. Characterization of heteroclite subgenomic RNAs associated with PRRSV infection. Virology. In press.
Zhou E-M, Jiang Z, Ameri-Mahabadi M, Zimmerman JJ. 2003. Detection and characterization of auto-anti-idiotypic antibodies specific for Idiotypic antibodies against envelope glycoprotein and matrix protein of porcine reproductive and respiratory syndrome virus. J Virol Methods (in press).
Zimmerman J. Epidemiology and ecology. 2003. In: The Porcine Reproductive and Respiratory Syndrome Compendium: A comprehensive reference on PRRS for pork producers, veterinary practitioners, and researchers (2nd edition). Zimmerman JJ, Yoon K-J (eds). National Pork Board, Des Moines Iowa, pp.27-50.
Zimmerman J. Historical overview. 2003. In: The Porcine Reproductive and Respiratory Syndrome Compendium: A comprehensive reference on PRRS for pork producers, veterinary practitioners, and researchers (2nd edition). Zimmerman JJ, Yoon K-J (eds). National Pork Board, Des Moines Iowa, pp.1-6.
Zimmerman JJ, Yoon K-J (editors). 2003. PRRS Compendium: A comprehensive reference on PRRS for pork producers, veterinary practitioners, and researchers (2nd edition). National Pork Board, Des Moines, Iowa. 294 pages
PROCEEDINGS AND ABSTRACTS:
Callahan, J.D., J. Christopher-Hennings, T.A. Gay, M.E. Reos, Y.Fang, M. Dammen, A. Wasilk, J. Galeota, F.A. Osorio, M. Torremorell, W.M. Nelson and E.A. Nelson. 2003. Development, validation and commercialization of a real-time RT-PCR assay for the detection of Lelystad, European-like and US Porcine reproductive and respiratory syndrome viruses. 107th Annual Meeting of the American Assoc. of Vet. Lab. Diagnostitions, p. 142.
Carlson, D.L., A.N. Wasilk, Y. Fang, S.A.E. Marras, E.A. Nelson and J. Christopher-Hennings. 2002. Detection, differentiation and quantitation of PRRSV strains by real-time RT-PCR with molecular beacons. 83rd Conf. of Research Workers in Animal Disease.
Christopher-Hennings, J., J. Callahan, T. Gay, A. Wasilk, Y. Fang, M. Dammen, M. Torremorell, D. Polson, M. Mellencamp, E.A. Nelson and W.M. Nelson. 2003. Validation of a real-time, quantitative PCR assay to detect U.S. and Lelystad/European-like PRRSV in boar semen and serum. 84th Conf. of Research Workers in Animal Disease.
Faaberg KS, Murtaugh MP, Mahlum-Wees CE, Johnson JE, Dwan C. 2003. Evolution of ORF5 in North America over 15 years. Proc. IXth International Symposium of Nidoviruses. 4.4, Egmond aan Zee, The Netherlands.
Faaberg, K. S., Murtaugh, M. P., Mahlum-Wees, C. E., Johnson, J. E., and C. Dwan. 2003. PRRSV: Evolution of ORF5 in North America over 15 years. IXth International Symposium on Nidoviruses,
Fang, Y., D. Kim, R.R.R. Rowland, S. Ropp, P. Steen, J. Christopher-Hennings and E.A. Nelson. 2003. Heterogeneity in the NSP2 gene of European-like PRRSV isolated in the United States. 84th Conf. of Research Workers in Animal Disease.
Fang, Y., W.P. Zhang, R.R.R. Rowland, J. Christopher-Hennings and E.A. Nelson. 2003. Phylogeny of European-like PRRSV isolates in North America. 84th Conf. of Research Workers in Animal Disease.
Ferrin, N.H., Y. Fang, D.D. Polson, M. Torremorell, M. Gramer, M.P. Murtaugh, C.R. Johnson, and E.A. Nelson. 2002. Validation of a blocking ELISA for antibodies against PRRSV. 83rd Conf. of Research Workers in Animal Disease.
Goldberg, T. L., J. F. Lowe, S. M. Milburn, L. D. Firkins. 2003. Quasispecies diversity of porcine reproductive and respiratory syndrome virus during natural infection. CRWAD 2003 Proceedings. ISU Press. Abst 153.
Hadley, L., Xu, J-S., McCaw, M.B., and Laster, S. 2002. Purified proteins from an acute strain of PRRSv provide protection via TH1-type immune response. In: Proceedings of 17th Congress of the International Pig Veterinary Society, Ames, Iowa, USA.
Liu, G., Nielsen, H. S., Burkhart, K. M., Roof, M. B., Vaughn, E. M., and K. S. Faaberg. 2003. Porcine Respiratory and Reproductive Syndrome Virus (PRRSV) Infectious Clones Reveal Nucleotides Important for Genome Replication. IXth International Symposium on Nidoviruses, P.6.6, Egmond aan Zee, The Netherlands.
Liu, G., Nielsen, H. S., Zhiming, O., and K. S. Faaberg. 2003. Infectivity of porcine respiratory syndrome virus genomic clones. 21th Annual Meeting of the American Society for Virology, W14-5, Davis, CA.
Lowe J.F., L.D. Firkins, F. A. Zuckerman, T.L. Goldberg. 2003. Immune response and reproductive performance in swine following known infection with PRRS virus in commercial herds. CRWAD 2003 Proceedings. ISU Press. Abst 144.
McCaw, M.B. Roberts, J, Laster, S.M., Hadley, L., and Erickson, G.A. 2003. Characterization of PRRSv antibody and rtPCR responses following repeated exposures and then challenge with homologous wild-type virus. In: Proceedings of 4th International Symposium on Emerging and Re-emerging Pig Diseases, Rome, Italy. pp 81-82.
McCaw, M.B., J. Roberts, J.J. Zimmerman, Laster, S., Hadley, L.,G.A. Erickson. 2002. PRRSv ELISA response and PCR viremia following repeated homologous exposures to wild-type virus in adult swine. Conference in Research Workers in Animal Disease. St. Louis, MO.
McCaw, M.B., Roberts, J., Laster, S., Hadley, L., and Erickson, G.A. 2002. PRRSv serologic assay limitations following repeated homologous exposures to wild-type virus in adult swine. In: Proceedings of 17th Congress of the International Pig Veterinary Society, 2002, Ames, Iowa, USA. p208.
Mondaca-Fernandez E, Morrison RB, Murtaugh MP. 2003. Using GIS and sequencing to assess regional epidemiology of PRRSV. Proc. Allen D. Leman Swine Conf. 30:71-74.
Murtaugh MP, Harding J, Faaberg KS. 2003. Genetic variation and biological safety of Ingelvac MLV modified live PRRS vaccine during seven years of continuous use in the field. 4th International Symposium on Emerging and Re-emerging Pig Diseases. Rome.
Murtaugh MP, Harding J. 2003. PRRS virus genomics: application to a field investigation. Proc. Allen D. Leman Swine Conf. 30:41-43.
Murtaugh MP, Wees CE, Johnson JE, Dwan C,Faaberg KS. 2003. Molecular evolution of porcine reproductive and respiratory syndrome virus (PRRSV) envelope glycoprotein 5. 4th International Symposium on Emerging and Re-emerging Pig Diseases. Abstract 57. Rome.
Murtaugh MP, Xiao Z, Johnson CR, Dee SA Batista L. 2003. Porcine immunity to porcine reproductive and respiratory syndrome virus (PRRSV): systemic and local responses in acute and persistent infection. Proc. IXth International Symposium of Nidoviruses
Petry DB, Holl JW, Weber J, Doster AR, Osorio FA, and RK Johnson. 2004. Different biological responses of pigs of two genetic populations to PRRSV challenge suggests underlying genetic variation in susceptibility/resistance to PRRSV, Nebraska Swine Report (In press)
Roof, M. B., Vaughn, E. M., Burkhart, K. M., and K.S. Faaberg. 2003. Efficacy of modified live virus porcine reproductive and respiratory virus vaccines against heterologous respiratory challenge. 4th International Symposium on Emerging and Re-emerging Pig Diseases: PRRS, PMWS, Swine Influenza. Abstract 15, 45-16, Rome, Italy.
Ropp, S.L., Y. Fang, M. Bien, B. Arndt, S. Preszler, P. Steen, J. Christopher-Hennings, D.A. Benfield and E. A. Nelson. 2002. Antigenic and genetic characterization of emerging European-like PRRSV isolates in the United States. 83rd Conf. of Research Workers in Animal Disease.
Royaee A, F.A. Zuckermann, R. Husmann, G. Calzada-Nova, W. Schnitzlein, J.K. Lunney. 2003. T cell cytokine response and gene expression profile of porcine lymphoid cells in response to vaccination with PRRS virus. CRWAD 2003 Proceedings. ISU Press. Abst. 115.
Thacker E, Kittikoon P, Vincent A, Hipple K, Nilubol D, Yu S, Janke B, Thacker B. 2003. Influence of PRRS virus infection on swine influenza vaccine efficacy. Emerging Disease Conference, Rome, Italy.
Vincent A, Thacker B, Halbur P, Rothschild M, Thacker E. 2003. An investigation of susceptibility to porcine reproductive and respiratory syndrome virus between genetically diverse lines of pigs. CRWAD, Chicago, Il Nov 10, 2003.
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