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: 11/01/2001 to 11/01/2002
- Date of Report: 12/06/2002
- Annual Meeting Dates: 11/09/2002 to 11/09/2002
Participants
[Minutes]
Accomplishments
Abbreviated.
Objective 1. MN, with the Danish Veterinary Institute, produced an infectious clone of strain VR-2332. Cytopathic effect (CPE) was seen only after several passages in MARC145 cells. MO, focusing on different potential pitfalls as compared to MN, cloned isolate NADC8. Transfections gave viral growth after 2-3 blind passages. Transfection supernatants injected into naove pigs yielded weakly positive serum, but none of the pigs seroconverted. ND and SD, with Guelph University (Canada), generated a clone of SD23983 that was not infectious. Clones were exchanged and are being used to generate chimeras in an effort to create an infectious clone. Nonstructural protein (nsp)-specific sera were generated, and obtained from Leiden Univ, the Netherlands, for detection of early viral nonstructural proteins to aid in troubleshooting. An equine arteritis virus (EAV) infectious clone was provided by Leiden Univ as a positive control.
SD and ND showed that field strains adapted to grow to high titers in MARC-145 cells were markedly reduced for growth in macrophages. Sequencing of MARC-145-adapted and nonadapted strains is underway to identify attenuation-related mutations. ND is using EAV as a surrogate to develop assays to compare replicative properties of more- and less-virulent PRRSV strains. Advancements were made to quantify transcript accumulation, transcript stability, replicase subunit accumulation, and replicase subunit stability.
KA, with Guelph University, showed that nucleocapsid (N)-eGFP fusion protein localizes to the nucleolus. Individual functional domains were also identified for a cryptic nuclear localization signal (NLS), NLS-1, at amino acid 10, a legitimate NLS, NLS-2, at amino acid 41, a cytoplasmic localization domain adjacent to NLS-2, and a potential nuclear export signal (NES) at amino acid 106. The results suggest that intracellular trafficking of N involves nuclear import, export and cytoplasmic retention signal sequences.
KA reported that amino acids 34-53 of N bind the 5-leader of PRRSV. The RNA-binding sequence is conserved and is unique to PRRSV. KA also reported interactions of cellular proteins from nonpermissive BHK-21 and permissive MARC145 cells with the positive strand of the 3-untranslated region (UTR) and ORF 7 RNA. Virus titer was reduced by 98% by a monoclonal antibody against PRRSV binding proteins of 210, 80, 55, and 30 kDa, indicating a possible receptor complex for PRRSV. CD151, a tetraspan family member, was identified by KA as binding PRRSV 3-RNA. It made BHK-21 cells permissive to PRRSV, suggesting that the CD151 is a susceptibility factor for PRRSV infection.
To explore possible mechanisms for the emergence of acute PRRS in 1996-97, the ORF5 gene of eight acute PRRSV isolates from herds in Iowa and North Carolina was sequenced (VA). They shared 87-97% nucleotide sequence identities with North American PRRSV isolates and vaccines. Isolate 98-37120-2 from a non-vaccinated herd in Iowa was very close to Ingelvac PRRS MLV. The other seven isolates were more related to earlier PRRSV isolates and PrimePac vaccine. The data do not fully support the hypothesis that acute PRRS is due to reversion of vaccines to a pathogenic phenotype. IA and VA collaborated on comparison of recent PRRSV field isolates to Ingelvac PRRS MLV vaccine, and its parent strain, VR2332. The results indicated that vaccine-like isolate 98-38803 is a derivative of Ingelvac PRRS MLV and that the isolate is pneumovirulent.
Low virulent isolates of PRRSV and porcine respiratory coronavirus together enhance respiratory disease and lesions (IA). IA and VA also showed that circovirus-2 infection increases the severity of PRRSV-induced interstitial pneumonia and that circovirus-2, but not PRRSV, induces pathology characteristic of postweaning multisystemic wasting syndrome (PMWS).
Objective 2. Mechanisms of transmission that facilitate PRRSV area spread and persistence in the environment were studied by MN under conditions that replicated commercial swine management practices and building design. Airborne transmission occurred across an airspace of 2 meters, but did not occur from within the facility to swine housed 1 meter outside and directly in line with an exhaust fan. Routing exhaust air into a housing unit containing naive pigs also failed to produce infection or seroconversion. Neither Mallard ducks housed inside a facility with infected pigs, nor experimentally infected Mallard and Rouen ducks, seroconverted or become viremic (MN, SD, IA, NE).
Mechanical transmission of PRRSV by mosquitoes and houseflies occurred when they were fed on infected pigs. Virus was retained in the midgut for 6-12 hr. Interruption of feeding, followed by exposure to naive pigs, resulted in transmission and infection in recipient pig. Fomites, including packed snow, also were demonstrated to mediate transmission of PRRSV into biosecure facilities. These findings demonstrate that PRRSV can be disseminated across considerable distances in a disconnected fashion in nonfreezing and freezing weather.
Viral persistence in pigs was studied by IA, NE, SD, MS, and IL. Animals on commercial farms were persistently infected and re-infected, and multiple viral types coexisted on farms (IL). The contribution of viral evolution to persistence in animals was studied by IA and MN. Multiple variants in ORF 5, but not ORFs 1b (replicase) and 7, were present concurrently in every pig. Most nucleotide changes in ORF5 resulted in substitution of amino acid residues. Virus mutation may not play a role in persistence, since overall genetic change was and there was no evidence of antigenic change (IA). PRRSV was detected in the tonsil of 5 of 8 boars that were negative in serum, semen and PBMC for 2-3 weeks (SD), but in 1 boar at 88 days post-inoculation, PRRSV could not be found by VI or PCR in any of 22 tissues, serum or semen.
Objective 3. To determine if multiple PRRSV exposure induced a state of nonresponsiveness in breeding age swine, pigs were infected with field virus following a 6/60 protocol widely used for sow vaccination (NC). 20% of 55 pigs returned to IDEXX ELISA seronegative status following six homologous wild-type virus infections, even though all pigs had initially seroconverted. Neutralizing antibody was detected in all animals throughout the study. 12 months after initial exposure, animals were infected with homolous (SD 23983) or heterologous (Powell) PRRSV. PRRSV was detected in some animals by PCR, suggesting that they were not fully protected. Only modest anamnestic ELISA and SN antibody responses were observed after homologous virus challenge, but marked increases occurred after heterologous challenge.
Several lines of evidence suggest that the immune response to PRRSV is weak. MN and IL showed that the cytokine IL-12 enhanced interferon (IFN) gamma responses of lymphocytes to PRRSV, and the mucosal adjuvant, cholera toxin, induced a robust antibody response to GP5. Further studies by IL and NE showed that co-delivery of IL-12 or porcine IFN alpha cDNA with PRRS MLV vaccine increased the primary PRRS-virus specific IFN gamma T cell response. Addition of IL-12 to a killed vaccine (PRRomise, Intervet) modestly increased IFN gamma response and antibody titers (IA). IL also showed that most pigs develop low or no titers of virus-neutralizing antibodies. A positive correlation was observed between the frequency of PRRS virus-specific IFN gamma secreting cells and the number of live-born pigs in immune-challenged sows (IL). In vaccinated sows at a commercial facility, only animals with a frequency of >150 PRRS virus-specific IFN gamma secreting cells per million PBMC did not abort following a natural outbreak of PRRS. The significance of the IFN gamma response is not fully understood, since there is a large variation in the response of individual pigs (IL and MN).
To evaluate the protective immune effect of structural proteins, pigs were immunized with Powell strain recombinant ORFs 2-5 (outer membrane proteins) and matrix protein (M) expressed in insect cells (NC). Vaccination with any of the recombinant proteins reduced levels of infectious virus, prevented fever, and prevented behavioral depression. Strong DTH reactions occurred against ORFs 4 and 5, the immunogens that reduced viral load most substantially. NE and IA identified an immunodominant, nonneutralizing epitope in GP5, and a different, neutralizing but non-immunodominant epitope that highly conserved among isolates. The nonneutralizing epitope may act as a decoy, eliciting most of the antibodies directed to GP5 and delaying the induction of neutralizing antibody. NE, IL, and SD collaborated on the construction and immunogenicity evaluation of Mycobacterium bovis BCG expressing GP5 and M proteins. Pigs developed specific immune response against the viral proteins, and 3 of 5 animals developed neutralizing antibodies. An IFN gamma response was not developed against the viral proteins. Following virulent challenge, immunized pigs showed shortened fever, lower viremia, and reduced virus in bronchial lymph nodes, consistent with protection.
KA, with Thomas Jefferson University, identified putative genetic suppressor elements (GSEs) in the PRRSV genome that may render cells permanently resistant to virus infection. Four sequences were identified; one encodes an antisense RNA matching the 5 end of ORF1b, and the others encode sense RNA matching sequences in nsp 11, ORF 2 and ORF 6.
Objective 4. SD and MN developed a blocking N ELISA. Sensitivity was 97.3% and specificity was 100%. CV was 4.12%. 147 of 4142 serum samples from PRRSV negative farms were unexpectedly positive by the IDEXX ELISA (SD, MN, IA). 100% of the 147 samples were negative by IFA and 97% were negative by blocking ELISA. Thus, blocking ELISA is an alternative to IFA for determining the PRRSV serostatus of individual animals. IA, SD, MN, KA, and NE determined that the rate of suspected-false- IDEXX-positive reactors is 0.5-2%. As IDEXX recently introduced a new version of PRRS ELISA, its diagnostic performance needs to be evaluated.
Serodiagnosis of European-genotype PRRSV in the US was improved by SD. European-like PRRSV isolates were grown for improved IFA and virus neutralization assays. 60 monoclonal antibodies recognized Lelystad virus-like isolates. One monoclonal antibody against N protein recognized the US European-genotype PRRSV isolates but not the Lelystad virus or other European isolates. Phylogenetic analysis of the structural protein sequences indicated that these isolates are typical European genotypes. Some of the unique characteristics of these European-like isolates can have a significant impact on diagnostic approaches to detecting PRRSV in US herds.
Current PRRS diagnostic tests were evaluated for detecting PRRSV infection in fetuses. PCR showed the best performance. Submission of whole litters and more than one litter is critical for accurate diagnosis as distribution of the virus among fetuses is not uniform (SD).
Quantitative, real-time PCR assays were developed for the detection of PRRSV by SD and MN. Probes that differentiate US and European PRRSV field and vaccine strains were made (SD). A heteroduplex mobility assay for rapid differentiation of vaccine-like viruses from field viruses was developed and compared to sequencing (VA, IA). The assay was shown to effectively detect and differentiate field isolates from vaccine strains. Isolates with 2% sequence divergence from the vaccine were all determined to be wild-type.
A porcine respiratory disease complex (PRDC) microarray is being developed to simultaneously diagnose PRRSV, influenza A, circovirus 2, Pasteurella multocida, Mycoplasma hyopneumoniae, Streptococcus suis, Actinobacillus pleuropneumoniae, Bordetella bronchiseptica, Haemophilus parasuis, Leptospira species, and porcine parvovirus (MN).
Objective 1. MN, with the Danish Veterinary Institute, produced an infectious clone of strain VR-2332. Cytopathic effect (CPE) was seen only after several passages in MARC145 cells. MO, focusing on different potential pitfalls as compared to MN, cloned isolate NADC8. Transfections gave viral growth after 2-3 blind passages. Transfection supernatants injected into naove pigs yielded weakly positive serum, but none of the pigs seroconverted. ND and SD, with Guelph University (Canada), generated a clone of SD23983 that was not infectious. Clones were exchanged and are being used to generate chimeras in an effort to create an infectious clone. Nonstructural protein (nsp)-specific sera were generated, and obtained from Leiden Univ, the Netherlands, for detection of early viral nonstructural proteins to aid in troubleshooting. An equine arteritis virus (EAV) infectious clone was provided by Leiden Univ as a positive control.
SD and ND showed that field strains adapted to grow to high titers in MARC-145 cells were markedly reduced for growth in macrophages. Sequencing of MARC-145-adapted and nonadapted strains is underway to identify attenuation-related mutations. ND is using EAV as a surrogate to develop assays to compare replicative properties of more- and less-virulent PRRSV strains. Advancements were made to quantify transcript accumulation, transcript stability, replicase subunit accumulation, and replicase subunit stability.
KA, with Guelph University, showed that nucleocapsid (N)-eGFP fusion protein localizes to the nucleolus. Individual functional domains were also identified for a cryptic nuclear localization signal (NLS), NLS-1, at amino acid 10, a legitimate NLS, NLS-2, at amino acid 41, a cytoplasmic localization domain adjacent to NLS-2, and a potential nuclear export signal (NES) at amino acid 106. The results suggest that intracellular trafficking of N involves nuclear import, export and cytoplasmic retention signal sequences.
KA reported that amino acids 34-53 of N bind the 5-leader of PRRSV. The RNA-binding sequence is conserved and is unique to PRRSV. KA also reported interactions of cellular proteins from nonpermissive BHK-21 and permissive MARC145 cells with the positive strand of the 3-untranslated region (UTR) and ORF 7 RNA. Virus titer was reduced by 98% by a monoclonal antibody against PRRSV binding proteins of 210, 80, 55, and 30 kDa, indicating a possible receptor complex for PRRSV. CD151, a tetraspan family member, was identified by KA as binding PRRSV 3-RNA. It made BHK-21 cells permissive to PRRSV, suggesting that the CD151 is a susceptibility factor for PRRSV infection.
To explore possible mechanisms for the emergence of acute PRRS in 1996-97, the ORF5 gene of eight acute PRRSV isolates from herds in Iowa and North Carolina was sequenced (VA). They shared 87-97% nucleotide sequence identities with North American PRRSV isolates and vaccines. Isolate 98-37120-2 from a non-vaccinated herd in Iowa was very close to Ingelvac PRRS MLV. The other seven isolates were more related to earlier PRRSV isolates and PrimePac vaccine. The data do not fully support the hypothesis that acute PRRS is due to reversion of vaccines to a pathogenic phenotype. IA and VA collaborated on comparison of recent PRRSV field isolates to Ingelvac PRRS MLV vaccine, and its parent strain, VR2332. The results indicated that vaccine-like isolate 98-38803 is a derivative of Ingelvac PRRS MLV and that the isolate is pneumovirulent.
Low virulent isolates of PRRSV and porcine respiratory coronavirus together enhance respiratory disease and lesions (IA). IA and VA also showed that circovirus-2 infection increases the severity of PRRSV-induced interstitial pneumonia and that circovirus-2, but not PRRSV, induces pathology characteristic of postweaning multisystemic wasting syndrome (PMWS).
Objective 2. Mechanisms of transmission that facilitate PRRSV area spread and persistence in the environment were studied by MN under conditions that replicated commercial swine management practices and building design. Airborne transmission occurred across an airspace of 2 meters, but did not occur from within the facility to swine housed 1 meter outside and directly in line with an exhaust fan. Routing exhaust air into a housing unit containing naive pigs also failed to produce infection or seroconversion. Neither Mallard ducks housed inside a facility with infected pigs, nor experimentally infected Mallard and Rouen ducks, seroconverted or become viremic (MN, SD, IA, NE).
Mechanical transmission of PRRSV by mosquitoes and houseflies occurred when they were fed on infected pigs. Virus was retained in the midgut for 6-12 hr. Interruption of feeding, followed by exposure to naive pigs, resulted in transmission and infection in recipient pig. Fomites, including packed snow, also were demonstrated to mediate transmission of PRRSV into biosecure facilities. These findings demonstrate that PRRSV can be disseminated across considerable distances in a disconnected fashion in nonfreezing and freezing weather.
Viral persistence in pigs was studied by IA, NE, SD, MS, and IL. Animals on commercial farms were persistently infected and re-infected, and multiple viral types coexisted on farms (IL). The contribution of viral evolution to persistence in animals was studied by IA and MN. Multiple variants in ORF 5, but not ORFs 1b (replicase) and 7, were present concurrently in every pig. Most nucleotide changes in ORF5 resulted in substitution of amino acid residues. Virus mutation may not play a role in persistence, since overall genetic change was and there was no evidence of antigenic change (IA). PRRSV was detected in the tonsil of 5 of 8 boars that were negative in serum, semen and PBMC for 2-3 weeks (SD), but in 1 boar at 88 days post-inoculation, PRRSV could not be found by VI or PCR in any of 22 tissues, serum or semen.
Objective 3. To determine if multiple PRRSV exposure induced a state of nonresponsiveness in breeding age swine, pigs were infected with field virus following a 6/60 protocol widely used for sow vaccination (NC). 20% of 55 pigs returned to IDEXX ELISA seronegative status following six homologous wild-type virus infections, even though all pigs had initially seroconverted. Neutralizing antibody was detected in all animals throughout the study. 12 months after initial exposure, animals were infected with homolous (SD 23983) or heterologous (Powell) PRRSV. PRRSV was detected in some animals by PCR, suggesting that they were not fully protected. Only modest anamnestic ELISA and SN antibody responses were observed after homologous virus challenge, but marked increases occurred after heterologous challenge.
Several lines of evidence suggest that the immune response to PRRSV is weak. MN and IL showed that the cytokine IL-12 enhanced interferon (IFN) gamma responses of lymphocytes to PRRSV, and the mucosal adjuvant, cholera toxin, induced a robust antibody response to GP5. Further studies by IL and NE showed that co-delivery of IL-12 or porcine IFN alpha cDNA with PRRS MLV vaccine increased the primary PRRS-virus specific IFN gamma T cell response. Addition of IL-12 to a killed vaccine (PRRomise, Intervet) modestly increased IFN gamma response and antibody titers (IA). IL also showed that most pigs develop low or no titers of virus-neutralizing antibodies. A positive correlation was observed between the frequency of PRRS virus-specific IFN gamma secreting cells and the number of live-born pigs in immune-challenged sows (IL). In vaccinated sows at a commercial facility, only animals with a frequency of >150 PRRS virus-specific IFN gamma secreting cells per million PBMC did not abort following a natural outbreak of PRRS. The significance of the IFN gamma response is not fully understood, since there is a large variation in the response of individual pigs (IL and MN).
To evaluate the protective immune effect of structural proteins, pigs were immunized with Powell strain recombinant ORFs 2-5 (outer membrane proteins) and matrix protein (M) expressed in insect cells (NC). Vaccination with any of the recombinant proteins reduced levels of infectious virus, prevented fever, and prevented behavioral depression. Strong DTH reactions occurred against ORFs 4 and 5, the immunogens that reduced viral load most substantially. NE and IA identified an immunodominant, nonneutralizing epitope in GP5, and a different, neutralizing but non-immunodominant epitope that highly conserved among isolates. The nonneutralizing epitope may act as a decoy, eliciting most of the antibodies directed to GP5 and delaying the induction of neutralizing antibody. NE, IL, and SD collaborated on the construction and immunogenicity evaluation of Mycobacterium bovis BCG expressing GP5 and M proteins. Pigs developed specific immune response against the viral proteins, and 3 of 5 animals developed neutralizing antibodies. An IFN gamma response was not developed against the viral proteins. Following virulent challenge, immunized pigs showed shortened fever, lower viremia, and reduced virus in bronchial lymph nodes, consistent with protection.
KA, with Thomas Jefferson University, identified putative genetic suppressor elements (GSEs) in the PRRSV genome that may render cells permanently resistant to virus infection. Four sequences were identified; one encodes an antisense RNA matching the 5 end of ORF1b, and the others encode sense RNA matching sequences in nsp 11, ORF 2 and ORF 6.
Objective 4. SD and MN developed a blocking N ELISA. Sensitivity was 97.3% and specificity was 100%. CV was 4.12%. 147 of 4142 serum samples from PRRSV negative farms were unexpectedly positive by the IDEXX ELISA (SD, MN, IA). 100% of the 147 samples were negative by IFA and 97% were negative by blocking ELISA. Thus, blocking ELISA is an alternative to IFA for determining the PRRSV serostatus of individual animals. IA, SD, MN, KA, and NE determined that the rate of suspected-false- IDEXX-positive reactors is 0.5-2%. As IDEXX recently introduced a new version of PRRS ELISA, its diagnostic performance needs to be evaluated.
Serodiagnosis of European-genotype PRRSV in the US was improved by SD. European-like PRRSV isolates were grown for improved IFA and virus neutralization assays. 60 monoclonal antibodies recognized Lelystad virus-like isolates. One monoclonal antibody against N protein recognized the US European-genotype PRRSV isolates but not the Lelystad virus or other European isolates. Phylogenetic analysis of the structural protein sequences indicated that these isolates are typical European genotypes. Some of the unique characteristics of these European-like isolates can have a significant impact on diagnostic approaches to detecting PRRSV in US herds.
Current PRRS diagnostic tests were evaluated for detecting PRRSV infection in fetuses. PCR showed the best performance. Submission of whole litters and more than one litter is critical for accurate diagnosis as distribution of the virus among fetuses is not uniform (SD).
Quantitative, real-time PCR assays were developed for the detection of PRRSV by SD and MN. Probes that differentiate US and European PRRSV field and vaccine strains were made (SD). A heteroduplex mobility assay for rapid differentiation of vaccine-like viruses from field viruses was developed and compared to sequencing (VA, IA). The assay was shown to effectively detect and differentiate field isolates from vaccine strains. Isolates with 2% sequence divergence from the vaccine were all determined to be wild-type.
A porcine respiratory disease complex (PRDC) microarray is being developed to simultaneously diagnose PRRSV, influenza A, circovirus 2, Pasteurella multocida, Mycoplasma hyopneumoniae, Streptococcus suis, Actinobacillus pleuropneumoniae, Bordetella bronchiseptica, Haemophilus parasuis, Leptospira species, and porcine parvovirus (MN).
Impacts
- An infectious clone will provide both a direct method for studying the role of viral genes in the pathogenesis of PRRSV as well as the development of a genetically-engineered marker vaccine.
- Transmission studies that confirm previous observations of limited airborne and avian spread of PRRSV, combined with demonstrations of fomite and insect-born spread of virus to biosecure facilities, address producer concerns about the inability to effectively prevent PRRSV introduction to noninfected herds by showing that current practices may not be sufficient.
- Studies of genetic variation during persistent infection of animals shows that PRRSV persistence is not dependent on immune evasion or neutralization escape. It increases the likelihood that persistence in animals is due, at least in part, to a weak immune response.
- Antibody and T lymphocyte responses are both important for an effective immune response to PRRSV. More specific immune assays that measure functionally relevant responses to defined antigens are expected to identify improved correlates of protective immunity to acute and persistent infection. These findings will facilitate development of more efficacious vaccines.
- The blocking ELISA to resolve false-positive serology directly addresses a critical producer concern. Reagent development for serological diagnosis of European-like field cases further enhances the accuracy and reliability of PRRS serology.
- Direct, rapid and sensitive PCR tests for infection status that differentiate US and European genotypes and distinguish between field and vaccine isolates will provide producers and veterinarians will greatly improved tools to assess the infection or protection status of herds and individual breeding animals.
- Plans for the group are to develop a public, international workshop on PRRS advances, publish literature reviews built around the four programmatic objectives, and to investigate development of an international scientific training program for PRRS research.
Publications
Does not include abstracts, proceedings, or lay publications.
Bastos RG, Dellagostin O, Barletta R, Doster A, Nelson E, Lopez O, Osorio FA. 2002. Construction and immunological evaluation of M. bovis BCG expressing GP5 and M protein of porcine reproductive respiratory syndrome virus, Vaccine (In Press)
Batista L, Dee SA, Rossow KD, Deen J, Pijoan C. 2002. An assessment of PRRV persistence and shedding in a large population of breeding age female swine. Can J Vet Res 66:196-200.
Bautista EM, Faaberg, KS, MacGruder ED. 2002. Cloning and expression of PRRSV ORF1b and characterization of NTPase activity. Virology 298:258-270.
Benson JE, Yaeger MJ, Christopher-Hennings J, Lager K, Yoon K-J. 2002. A comparison of virus isolation, immunohistochemistry, fetal serology, and reverse transcriptase-polymerase chain reaction for the diagnosis of porcine reproductive and respiratory syndrome in the fetus. J Vet Diagn Invest 14:8-14.
Bierk MD, Dee SA, Rossow KD, Collins JE, Otake S, Molitor TW. 2001. Transmission of PRRS virus from persistently infected sows to contact controls. Can J Vet Res 65: 261-266.
Boettcher TB, Thacker BJ, Halbur PG, Waters WR, Nutsch R, Thacker EL. 2002. Vaccine efficacy and immune response to Mycoplasma hyopneumoniae challenge in pigs vaccinated against porcine reproductive and respiratory syndrome virus and M. hyopneumoniae. J Swine Hlth Prod 10:259-264.
Cancel-Tirado SM, Yoon K-J. 2002. Antibody dependent enhancement of virus infection and disease. Viral Immunol. (in press)
Chang CC, Yoon KJ, Zimmerman JJ, Harmon KM, Dixon PM, Dvorak CMT, Murtaugh MP. 2002. Evolution of porcine reproductive and respiratory syndrome (PRRS) virus during sequential passages in pigs. J Virol. 76:4750-4763.
Christopher-Hennings J, Faaberg KS, Mengeling WL, Murtaugh MP, Nelson EA, Roof MB, Vaughn EM, Yoon K-J, Zimmerman JJ. 2002. Porcine reproductive and respiratory syndrome (PRRS) diagnostics: Interpretation and limitations. J Swine Hlth Prod. 10:213-218.
Christopher-Hennings J, Holler LD, Benfield DA, Nelson EA. 2001. Detection and duration of porcine reproductive and respiratory syndrome virus in semen, serum, peripheral blood mononuclear cells and tissues from Yorkshire, Hampshire and Landrace boars. J Vet Diagn Invest. 13:133-142.
Cuatero L, Dee SA, Deen J, Ruiz A, and Pijoan C. 2002. Association between clinical signs and PRRSV viremia in nursery pigs under field conditions. Journal of Swine Hlthd Prod. 10:119-122.
Daginakatte GC, Kapil S. 2001. Fine mapping of the RNA binding domains of the porcine reproductive and respiratory syndrome virus nucleocapsid protein. Adv Expt Med Biol. 494:547-552.
Dee SA, Deen J. 2001. Establishment of a PRRS ELISA-negative boar population using previously exposed boars. Vet Rec 149: 678-680.
Dee SA, Deen J, Rossow KD, Mahlum C, Otake S, Joo HS, C Pijoan. 2002. Mechanical transmission of porcine reproductive and respiratory syndrome virus throughout a coordinated sequence of events during cold weather. Can J Vet Res (In press).
Dee SA, Torremorell M, Rossow K, Mahlum C, Otake S, and Faaberg K. 2001. Identification of genetically diverse sequences (ORF 5) of PRRSV in a swineherd. Can J Vet Res. 65:254-260.
Fairbanks K, Chase C, Benfield DA. 2002. Tonsil biopsies and polymerase chain reaction assay for detection of breeding age gilts persistently infected with porcine reproductive and respiratory syndrome virus. J Swine Hlth Prod. 10:1-2.
Feng W, Laster SM, Tompkins M, Brown TT, Xu J-S, Gomez W, Benfield D, 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.
Foss DL, Zilliox MJ, Meier W, Zuckermann F, Murtaugh MP. 2002. Adjuvant danger signals increase the immune response to porcine reproductive and respiratory syndrome virus. Viral Immunol. 15:557-566.
Halbur PG, Pallares FJ, Rathje JA, Evans R, Hagemoser WA, Paul PS, Meng XJ. 2002. Effects of different U.S. isolates of porcine reproductive and respiratory syndrome virus (PRRSV) on blood and bone marrow parameters of experimentally infected pigs. Vet Rec 151:344-348.
Hermann JR, Honeyman MS, Zimmerman JJ, Thacker BJ, Holden PJ, Chang CC. 2002. Effect of dietary Echinacea purpurea on viremia and performance in porcine reproductive and respiratory syndrome virus-infected nursery pigs. J An Sci (submitted).
Horter D, Chang CC, Pogranichnyy R, Zimmerman J, Yoon KJ. 2001. Persistence of porcine reproductive and respiratory syndrome in pigs. Adv Exp Med Biol. 494:91-94.
Horter DC, Pogranichniy RM, Chang C-C, Evans RB, Yoon K-J, Zimmerman JJ. 2002. Characterization of the carrier state in porcine reproductive and respiratory syndrome virus infection. Vet Microbiol. 86:213-228.
Hurd HS, Bush EJ, Losinger W, Corso B, Zimmerman JJ, Wills R, Swenson S, Pyburn D, Yeske P, Burkgren T. 2001. Outbreaks of porcine reproductive failure: report on a collaborative field investigation. J Swine Hlth Prod. 9:103-108.
Key KF, Haqshenas G, Guenette D, Swenson SL, Toth TE, Meng XJ. 2001. Genetic characterization of the major envelope gene of acute porcine reproductive and respiratory syndrome virus isolates. Vet Micro. 83:249-263.
Key KF, Guenette DK, Yoon KJ, Halbur PG, Vaughn EM, Roof M, Toth TE, Meng XJ. 2002. Identification and differentiation of vaccine-like isolates of porcine reproductive and respiratory syndrome virus from field isolates using a heteroduplex mobility assay. J Clin Micro. In press.
Kim TS, Benfield DA, Rowland RRR. 2002. Porcine reproductive and respiratory syndrome virus-induced cell death exhibits features consistent with a non-typical form of apoptosis. Virus Res. 85:133-140.
Kleiboeker SB, Lehman JR, Fangman TJ. 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 Hlth Prod. 10:251-258.
Majhdi F, Kapil S. 2001. Interactions of cellular proteins with the positive strand of 3‘ untranslated RNA and the nucleoprotein gene of porcine reproductive and respiratory syndrome virus. Adv Expt Med Biol. 494:633-639.
Meier WA, Galeota J, OsorioFA, Husmann RJ, Schnitzlein W, Zuckermann FA. 2003. Gradual development of the interferon-gamma and antibody responses of swine to porcine reproductive and respiratory syndrome virus. Virology In press.
Murtaugh MP, Yuan S, Nelson EA, Faaberg KS. 2002. Genetic interaction between porcine reproductive and respiratory syndrome virus (PRRSV) strains in cell culture and in animals. J Swine Hlth Prod. 10:15-21.
Murtaugh MP, Foss DL. 2002. Inflammatory cytokines and antigen presenting cell activation. Vet Immunol Immunopathol. 87:109-122.
Murtaugh MP, Xiao Z, Zuckermann F. 2002. Immunological responses of swine to porcine reproductive and respiratory syndrome virus infection. Viral Immunol. 15:533-547.
Murtaugh MP, Yaun S, Nelson EA, Faaberg KS. 2002. Genetic interaction between PRRSV strains in cell culture and in animals. J Swine Hlth Prod. 10:15-21.
Murtaugh MP, Xiao Z, Rutherford MS, Zuckermann F. 2002. Immunology. The Porcine Reproductive and Respiratory Syndrome (Porcine Arterivirus) Compendium (2nd Edition). Section 5.3. 28 pp. National Pork Board, Clive, Iowa. In press.
Nielsen HS, Liu GP, Nielsen J, Oleksiewicz MB, Bxtner A, Storgaard T, Faaberg KS. 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. In press.
Opriessnig T, Halbur PG, Yoon K-J, Pogranichniy RM, Harmon KM, Evans R, Key KF, Pallares FJ, Thomas P, Meng X-J. 2002. Comparative pathogenicity 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 FA, Galeota JA, Nelson E, Brodersen B, Doster A, Wills R, Zuckermann F, Laegreid WW. 2002. Passive transfer of virus -specific 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.
Ostrowski M, Galeota JA, Jar AM, Platt KB, Osorio FA, Lopez OJ. 2002 .Identification of neutralizing and non-neutralizing epitopes in the porcine reproductive and respiratory syndrome virus GP5 ectodomain. J Virol. 76:4241-50.
Otake S, Dee SA, Jacobson L, Torremorell M, and Pijoan C. 2002. Evaluation of aerosol transmission of porcine reproductive and respiratory syndrome virus under field conditions. Vet Rec. 150:804-808.
Otake S, Dee SA, Rossow KD, Deen J, Joo HS, Molitor TW, Pijoan C. 2002. Transmission of porcine reproductive and respiratory syndrome virus by fomites (boots and coveralls). J Swine Hlth Prod. 10: 59-65.
Otake S, Dee SA, Rossow KD, Deen J, Joo HS, Molitor TW, Pijoan C. 2002. Transmission of PRRSV by needles. Vet Rec. 150:114-115.
Otake S, Dee SA, Rossow KD, Moon RD, Pijoan C. 2002. Mechanical transmission of porcine reproductive and respiratory syndrome virus by mosquitoes, Aedes vexans (Meigen). Can J Vet Res. 66:191-195.
Otake S, Dee SA, Rossow KD, Moon RD, Trincado C, Pijoan C. 2003. Transmission of porcine reproductive and respiratory syndrome virus by houseflies (Linneaus). Vet Rec. In press.
Pallares FJ, Halbur PG, Opriessnig T, Sorden SD, Villar D, Janke BH, Yaeger MJ, Larson DJ, Schwartz KJ, Yoon KJ, Hoffman LJ. 2002. Porcine circovirus type 2 (PCV-2) co-infections in U.S. field cases of postweaning multisystemic wasting syndrome (PMWS). J Vet Diagn Invest. 14:515-519.
Pallares FJ, Halbur PG, Opriessnig T, Vaughn EM, Paul PS. 2002. Effects of dual infection of SPF pigs with low virulent isolates of porcine respiratory coronavirus (PRCV) and porcine reproductive and respiratory syndrome virus (PRRSV). Anaporc Cientifico 2:8-13.
Plagemann PGW, Rowland RRR, FaabergKS. 2002. The primary neutralization epitope of porcine reproductive and respiratory syndrome virus strain VR-2332 is located in the middle of the GP5 ectodomain. Arch Virol. 147:2327-2347.
Pogranichnyy RM, Yoon K-J, Harm PA, Sorden S, Daniels M. 2002. Case-control study on the association of porcine circovirus type 2 and other swine viruses in postweaning multisystemic wasting syndrome. J Vet Diagn Invest. 14:449-456.
Rowland R, Schneider P, Fang Y, Wootton S, Yoo D, Benfield DA. 2003. Peptide domains involved in the trafficking of the porcine reproductive and respiratory syndrome virus nucleocapsid protein. Virology. In press.
Wagstrom EA, Chang CC, Yoon KJ, Zimmerman JJ. 2001. Shedding of porcine reproductive and respiratory syndrome virus in mammary gland secretions of sows. Am J Vet Res. 62:1876-1880.
Wills RW, Doster AR, Galeota JA, Sur JH, Osorio FA. 2003. Duration of infection and proportion of pigs persistently infected with porcine reproductive and respiratory syndrome virus (PRRSV). J Clin Micro. In press.
Wills RW, Doster AR, Osorio FA. 2002. Transmission of porcine reproductive and respiratory syndrome virus (PRRSV) to age-matched sentinel pigs. J Swine Hlth Prod. 10:161-165.
Wootton SK, Rowland RR, Yoo D. 2002. Phosphorylation of the porcine reproductive and respiratory syndrome virus (PRRSV) nucleocapsid protein. J Virol. 76:10569-10576.
Yoon K-J, Christopher-Hennings J, Nelson EA. 2002. Diagnosis. In: Porcine Reproductive and Respiratory Syndrome (Porcine Arterivirus) Compendium (2nd Edition). National Pork Board, Clive, Iowa. In press.
Yoon K-J, Stevenson G. 2002. Porcine reproductive and respiratory syndrome: Diagnosis. In: Morilla A, Yoon KJ, Zimmerman JJ (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: Morilla A, Yoon KJ, Zimmerman JJ (eds). Trends in Emerging Viral Infections of Swine, pp 339-346. Iowa State University Press, Ames, Iowa
Yoon K-J. 2002. Virology. In: The Porcine Reproductive and Respiratory Syndrome (Porcine Arterivirus) Compendium (2nd edition). Zimmerman JJ (ed). National Pork Board, Des Moines Iowa (in press).
Zimmerman J. 2002. Epidemiology. In: The Porcine Reproductive and Respiratory Syndrome (Porcine Arterivirus) Compendium (2nd edition). Zimmerman JJ (ed). National Pork Board, Des Moines Iowa (in press).
Zimmerman J. 2002. A short history of porcine reproductive and respiratory syndrome. In: The Porcine Reproductive and Respiratory Syndrome (Porcine Arterivirus) Compendium (2nd edition). Zimmerman JJ (ed). National Pork Board, Des Moines Iowa (in press).
Zimmerman JJ. 2002. Porcine reproductive and respiratory syndrome virus epidemiology. In: Morilla A, Yoon K-J, Zimmerman J (eds). Trends in Emerging Viral Infections of Swine. Iowa State Press, Ames, Iowa, pp. 331-337.
Bastos RG, Dellagostin O, Barletta R, Doster A, Nelson E, Lopez O, Osorio FA. 2002. Construction and immunological evaluation of M. bovis BCG expressing GP5 and M protein of porcine reproductive respiratory syndrome virus, Vaccine (In Press)
Batista L, Dee SA, Rossow KD, Deen J, Pijoan C. 2002. An assessment of PRRV persistence and shedding in a large population of breeding age female swine. Can J Vet Res 66:196-200.
Bautista EM, Faaberg, KS, MacGruder ED. 2002. Cloning and expression of PRRSV ORF1b and characterization of NTPase activity. Virology 298:258-270.
Benson JE, Yaeger MJ, Christopher-Hennings J, Lager K, Yoon K-J. 2002. A comparison of virus isolation, immunohistochemistry, fetal serology, and reverse transcriptase-polymerase chain reaction for the diagnosis of porcine reproductive and respiratory syndrome in the fetus. J Vet Diagn Invest 14:8-14.
Bierk MD, Dee SA, Rossow KD, Collins JE, Otake S, Molitor TW. 2001. Transmission of PRRS virus from persistently infected sows to contact controls. Can J Vet Res 65: 261-266.
Boettcher TB, Thacker BJ, Halbur PG, Waters WR, Nutsch R, Thacker EL. 2002. Vaccine efficacy and immune response to Mycoplasma hyopneumoniae challenge in pigs vaccinated against porcine reproductive and respiratory syndrome virus and M. hyopneumoniae. J Swine Hlth Prod 10:259-264.
Cancel-Tirado SM, Yoon K-J. 2002. Antibody dependent enhancement of virus infection and disease. Viral Immunol. (in press)
Chang CC, Yoon KJ, Zimmerman JJ, Harmon KM, Dixon PM, Dvorak CMT, Murtaugh MP. 2002. Evolution of porcine reproductive and respiratory syndrome (PRRS) virus during sequential passages in pigs. J Virol. 76:4750-4763.
Christopher-Hennings J, Faaberg KS, Mengeling WL, Murtaugh MP, Nelson EA, Roof MB, Vaughn EM, Yoon K-J, Zimmerman JJ. 2002. Porcine reproductive and respiratory syndrome (PRRS) diagnostics: Interpretation and limitations. J Swine Hlth Prod. 10:213-218.
Christopher-Hennings J, Holler LD, Benfield DA, Nelson EA. 2001. Detection and duration of porcine reproductive and respiratory syndrome virus in semen, serum, peripheral blood mononuclear cells and tissues from Yorkshire, Hampshire and Landrace boars. J Vet Diagn Invest. 13:133-142.
Cuatero L, Dee SA, Deen J, Ruiz A, and Pijoan C. 2002. Association between clinical signs and PRRSV viremia in nursery pigs under field conditions. Journal of Swine Hlthd Prod. 10:119-122.
Daginakatte GC, Kapil S. 2001. Fine mapping of the RNA binding domains of the porcine reproductive and respiratory syndrome virus nucleocapsid protein. Adv Expt Med Biol. 494:547-552.
Dee SA, Deen J. 2001. Establishment of a PRRS ELISA-negative boar population using previously exposed boars. Vet Rec 149: 678-680.
Dee SA, Deen J, Rossow KD, Mahlum C, Otake S, Joo HS, C Pijoan. 2002. Mechanical transmission of porcine reproductive and respiratory syndrome virus throughout a coordinated sequence of events during cold weather. Can J Vet Res (In press).
Dee SA, Torremorell M, Rossow K, Mahlum C, Otake S, and Faaberg K. 2001. Identification of genetically diverse sequences (ORF 5) of PRRSV in a swineherd. Can J Vet Res. 65:254-260.
Fairbanks K, Chase C, Benfield DA. 2002. Tonsil biopsies and polymerase chain reaction assay for detection of breeding age gilts persistently infected with porcine reproductive and respiratory syndrome virus. J Swine Hlth Prod. 10:1-2.
Feng W, Laster SM, Tompkins M, Brown TT, Xu J-S, Gomez W, Benfield D, 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.
Foss DL, Zilliox MJ, Meier W, Zuckermann F, Murtaugh MP. 2002. Adjuvant danger signals increase the immune response to porcine reproductive and respiratory syndrome virus. Viral Immunol. 15:557-566.
Halbur PG, Pallares FJ, Rathje JA, Evans R, Hagemoser WA, Paul PS, Meng XJ. 2002. Effects of different U.S. isolates of porcine reproductive and respiratory syndrome virus (PRRSV) on blood and bone marrow parameters of experimentally infected pigs. Vet Rec 151:344-348.
Hermann JR, Honeyman MS, Zimmerman JJ, Thacker BJ, Holden PJ, Chang CC. 2002. Effect of dietary Echinacea purpurea on viremia and performance in porcine reproductive and respiratory syndrome virus-infected nursery pigs. J An Sci (submitted).
Horter D, Chang CC, Pogranichnyy R, Zimmerman J, Yoon KJ. 2001. Persistence of porcine reproductive and respiratory syndrome in pigs. Adv Exp Med Biol. 494:91-94.
Horter DC, Pogranichniy RM, Chang C-C, Evans RB, Yoon K-J, Zimmerman JJ. 2002. Characterization of the carrier state in porcine reproductive and respiratory syndrome virus infection. Vet Microbiol. 86:213-228.
Hurd HS, Bush EJ, Losinger W, Corso B, Zimmerman JJ, Wills R, Swenson S, Pyburn D, Yeske P, Burkgren T. 2001. Outbreaks of porcine reproductive failure: report on a collaborative field investigation. J Swine Hlth Prod. 9:103-108.
Key KF, Haqshenas G, Guenette D, Swenson SL, Toth TE, Meng XJ. 2001. Genetic characterization of the major envelope gene of acute porcine reproductive and respiratory syndrome virus isolates. Vet Micro. 83:249-263.
Key KF, Guenette DK, Yoon KJ, Halbur PG, Vaughn EM, Roof M, Toth TE, Meng XJ. 2002. Identification and differentiation of vaccine-like isolates of porcine reproductive and respiratory syndrome virus from field isolates using a heteroduplex mobility assay. J Clin Micro. In press.
Kim TS, Benfield DA, Rowland RRR. 2002. Porcine reproductive and respiratory syndrome virus-induced cell death exhibits features consistent with a non-typical form of apoptosis. Virus Res. 85:133-140.
Kleiboeker SB, Lehman JR, Fangman TJ. 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 Hlth Prod. 10:251-258.
Majhdi F, Kapil S. 2001. Interactions of cellular proteins with the positive strand of 3‘ untranslated RNA and the nucleoprotein gene of porcine reproductive and respiratory syndrome virus. Adv Expt Med Biol. 494:633-639.
Meier WA, Galeota J, OsorioFA, Husmann RJ, Schnitzlein W, Zuckermann FA. 2003. Gradual development of the interferon-gamma and antibody responses of swine to porcine reproductive and respiratory syndrome virus. Virology In press.
Murtaugh MP, Yuan S, Nelson EA, Faaberg KS. 2002. Genetic interaction between porcine reproductive and respiratory syndrome virus (PRRSV) strains in cell culture and in animals. J Swine Hlth Prod. 10:15-21.
Murtaugh MP, Foss DL. 2002. Inflammatory cytokines and antigen presenting cell activation. Vet Immunol Immunopathol. 87:109-122.
Murtaugh MP, Xiao Z, Zuckermann F. 2002. Immunological responses of swine to porcine reproductive and respiratory syndrome virus infection. Viral Immunol. 15:533-547.
Murtaugh MP, Yaun S, Nelson EA, Faaberg KS. 2002. Genetic interaction between PRRSV strains in cell culture and in animals. J Swine Hlth Prod. 10:15-21.
Murtaugh MP, Xiao Z, Rutherford MS, Zuckermann F. 2002. Immunology. The Porcine Reproductive and Respiratory Syndrome (Porcine Arterivirus) Compendium (2nd Edition). Section 5.3. 28 pp. National Pork Board, Clive, Iowa. In press.
Nielsen HS, Liu GP, Nielsen J, Oleksiewicz MB, Bxtner A, Storgaard T, Faaberg KS. 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. In press.
Opriessnig T, Halbur PG, Yoon K-J, Pogranichniy RM, Harmon KM, Evans R, Key KF, Pallares FJ, Thomas P, Meng X-J. 2002. Comparative pathogenicity 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 FA, Galeota JA, Nelson E, Brodersen B, Doster A, Wills R, Zuckermann F, Laegreid WW. 2002. Passive transfer of virus -specific 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.
Ostrowski M, Galeota JA, Jar AM, Platt KB, Osorio FA, Lopez OJ. 2002 .Identification of neutralizing and non-neutralizing epitopes in the porcine reproductive and respiratory syndrome virus GP5 ectodomain. J Virol. 76:4241-50.
Otake S, Dee SA, Jacobson L, Torremorell M, and Pijoan C. 2002. Evaluation of aerosol transmission of porcine reproductive and respiratory syndrome virus under field conditions. Vet Rec. 150:804-808.
Otake S, Dee SA, Rossow KD, Deen J, Joo HS, Molitor TW, Pijoan C. 2002. Transmission of porcine reproductive and respiratory syndrome virus by fomites (boots and coveralls). J Swine Hlth Prod. 10: 59-65.
Otake S, Dee SA, Rossow KD, Deen J, Joo HS, Molitor TW, Pijoan C. 2002. Transmission of PRRSV by needles. Vet Rec. 150:114-115.
Otake S, Dee SA, Rossow KD, Moon RD, Pijoan C. 2002. Mechanical transmission of porcine reproductive and respiratory syndrome virus by mosquitoes, Aedes vexans (Meigen). Can J Vet Res. 66:191-195.
Otake S, Dee SA, Rossow KD, Moon RD, Trincado C, Pijoan C. 2003. Transmission of porcine reproductive and respiratory syndrome virus by houseflies (Linneaus). Vet Rec. In press.
Pallares FJ, Halbur PG, Opriessnig T, Sorden SD, Villar D, Janke BH, Yaeger MJ, Larson DJ, Schwartz KJ, Yoon KJ, Hoffman LJ. 2002. Porcine circovirus type 2 (PCV-2) co-infections in U.S. field cases of postweaning multisystemic wasting syndrome (PMWS). J Vet Diagn Invest. 14:515-519.
Pallares FJ, Halbur PG, Opriessnig T, Vaughn EM, Paul PS. 2002. Effects of dual infection of SPF pigs with low virulent isolates of porcine respiratory coronavirus (PRCV) and porcine reproductive and respiratory syndrome virus (PRRSV). Anaporc Cientifico 2:8-13.
Plagemann PGW, Rowland RRR, FaabergKS. 2002. The primary neutralization epitope of porcine reproductive and respiratory syndrome virus strain VR-2332 is located in the middle of the GP5 ectodomain. Arch Virol. 147:2327-2347.
Pogranichnyy RM, Yoon K-J, Harm PA, Sorden S, Daniels M. 2002. Case-control study on the association of porcine circovirus type 2 and other swine viruses in postweaning multisystemic wasting syndrome. J Vet Diagn Invest. 14:449-456.
Rowland R, Schneider P, Fang Y, Wootton S, Yoo D, Benfield DA. 2003. Peptide domains involved in the trafficking of the porcine reproductive and respiratory syndrome virus nucleocapsid protein. Virology. In press.
Wagstrom EA, Chang CC, Yoon KJ, Zimmerman JJ. 2001. Shedding of porcine reproductive and respiratory syndrome virus in mammary gland secretions of sows. Am J Vet Res. 62:1876-1880.
Wills RW, Doster AR, Galeota JA, Sur JH, Osorio FA. 2003. Duration of infection and proportion of pigs persistently infected with porcine reproductive and respiratory syndrome virus (PRRSV). J Clin Micro. In press.
Wills RW, Doster AR, Osorio FA. 2002. Transmission of porcine reproductive and respiratory syndrome virus (PRRSV) to age-matched sentinel pigs. J Swine Hlth Prod. 10:161-165.
Wootton SK, Rowland RR, Yoo D. 2002. Phosphorylation of the porcine reproductive and respiratory syndrome virus (PRRSV) nucleocapsid protein. J Virol. 76:10569-10576.
Yoon K-J, Christopher-Hennings J, Nelson EA. 2002. Diagnosis. In: Porcine Reproductive and Respiratory Syndrome (Porcine Arterivirus) Compendium (2nd Edition). National Pork Board, Clive, Iowa. In press.
Yoon K-J, Stevenson G. 2002. Porcine reproductive and respiratory syndrome: Diagnosis. In: Morilla A, Yoon KJ, Zimmerman JJ (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: Morilla A, Yoon KJ, Zimmerman JJ (eds). Trends in Emerging Viral Infections of Swine, pp 339-346. Iowa State University Press, Ames, Iowa
Yoon K-J. 2002. Virology. In: The Porcine Reproductive and Respiratory Syndrome (Porcine Arterivirus) Compendium (2nd edition). Zimmerman JJ (ed). National Pork Board, Des Moines Iowa (in press).
Zimmerman J. 2002. Epidemiology. In: The Porcine Reproductive and Respiratory Syndrome (Porcine Arterivirus) Compendium (2nd edition). Zimmerman JJ (ed). National Pork Board, Des Moines Iowa (in press).
Zimmerman J. 2002. A short history of porcine reproductive and respiratory syndrome. In: The Porcine Reproductive and Respiratory Syndrome (Porcine Arterivirus) Compendium (2nd edition). Zimmerman JJ (ed). National Pork Board, Des Moines Iowa (in press).
Zimmerman JJ. 2002. Porcine reproductive and respiratory syndrome virus epidemiology. In: Morilla A, Yoon K-J, Zimmerman J (eds). Trends in Emerging Viral Infections of Swine. Iowa State Press, Ames, Iowa, pp. 331-337.