Brief Summary of Minutes of Annual Meeting

1.1 PRRSV Sequence Database. A web-accessible MySQL database was developed by UMN with funding from the National Pork Board (NPB) and SDSU. The web-site (http://prrsv.ahc.umn.edu) contains 5400 PRRSV ORF5 nucleotide sequences generated at MN and associated history, sequence and RFLP pattern. Up to 25 isolates can be multi-sequence aligned for further phylogenetic analysis using tools available at the same site, including ClustalX, Jalview and PFAAT. The effort was aimed at producing an easy to use database for nucleotide sequence mining.

1.2 Data sharing and analysis. The multi-institutional "Big Pig" project (KSU, ISU, SDSU, BARC, IDEXX) supplied thousands of biological samples at no charge to several other laboratories. It continues to distribute samples to researchers. All labs have participated in the movement toward a virtual laboratory through involvement in the development of ARM-7 database.

1.3 The PRRS virus isolate bank that was established will continue to be maintained at UMO.

1.4 Recombinant PRRSV polypeptides from strain VR2332 encoding portions of nonstructural protein 2 (nsp2), envelope glycoprotein 5 (GP5), and nucleocapsid (N) were produced at UMN with funds from NPB and are available to all PRRS investigators. Recombinant proteins encoding the nsp1, 7, 8, 12, and functional domains of nsp 2, 4, 9, 10, and 11 were in vitro expressed in E. coli by SDSU researchers. A full panel of monoclonal antibodies (mAbs) against PRRSV nsps is being developed at SDSU to study protein structure-function and design antiviral intervention strategies. A panel of mAbs against nsp1, 2, 3, 4, 7 and 8 were produced and screened by indirect immunofluorescence against and Western blotting or immunoprecipitation; other mAbs are in progress. These are basic reagents for study of the fundamental biology of PRRSV nsps and good candidates for future development of diagnostic assays.

1.5 Oligonucloetide microarray. PRRS-CAP 1 has collaborated with NPB and the national swine genome project (NRSP-8) to acquire a copy of the swine oligonucleotide array http://www.pigoligoarray.org/, that will facilitate functional genomic studies to better understand the virus-pig interaction and identify targets of immunological and pathogenic significance.

Objective 2. Achieve biosecurity within herds by preventing the spread of virus within a herd and facilitating its elimination from endemically infected herds. Research is focused on functional genomics of PRRSV resistance, mechanisms of protective immunity for PRRSV prevention, evaluation of immunomodulators to stimulate/enhance antiviral immunity and agents that reduce virus replication in the pig.

2.1 Cells of the immune system.

Flow cytometric and fluorescent antibody analysis of PRRSV infection of MARC-145 cells were used by SDSU scientists to clarify viral dynamics and the mechanism of viral spread. The roles of viral permissiveness and the cytoskeleton in PRRSV infection and transmission were examined in conjunction with antiviral and cytotoxic drugs. PRRSV infection and cell-to-cell transmission were efficiently suppressed by interferon-gamma (IFNg), and the more potent antiviral agent AK-2, indicating that an intact cytoskeleton is critical for PRRSV infection and that viral permissiveness is an efficient drug target.
KSU is mapping T-cell epitopes on PRRSV proteins. Using mesenteric lymph nodes (MLN) they determined that activated T cells co-express CD25 and MHC II on CD4+ T cells. Polyclonal activation and antigenic stimulation increased IFNg secreting cells. Fluorescent cell sorting-based assays have been adapted for the identification of T cell epitopes in PRRSV proteins. A peptide epitope of PRRSV GP5 stimulates IFNg secretion and CD4+ T cell proliferation. This information is critical for vaccines that assure stimulation of cell mediated immunity.
Plasmacytoid dendritic cells (PDC) are the most potent source of IFNa and thus are primarily responsible for the initial anti-viral protective response. UIUC scientists evaluated the behavior of pig PDC exposed to PRRSV both in vitro and in vivo. When freshly purified PDC were incubated with PRRSV, the resultant IFNa response was meager, much less intense than that stimulated by transmissible gastroenteritis virus (TGEV). That PRRSV affected PDC function was affirmed since it repressed the vigorous IFNa responsiveness to TGEV of PBMC. A similar impact of PRRSV on PDC was observed in vivo and may be unique since it was not found when swine were infected with Pseudorabies virus.

2.2 Cytokines.

BARC provided immune gene expression analyses for several projects including: 1) Testing immune gene expression in samples from PRRSV infected boars with SDSU; 2) With UIUC and NCSU, assessing in vitro test parameters (time in culture, PRRSV antigen) that produce the maximum immune gene expression data; 3) Comparing immune gene expression of pigs infected or vaccinated with type 1 and type 2 PRRSV with SDSU; and 4) Assessing the genetic basis of response by testing how different genetic lines of pigs respond to PRRSV with UNL. Results from these studies may explain why and how PRRSV infection modulates the immune response.
An early warning biomarker of infection would improve diagnosis and facilitate better PRRSV preventive strategies. UMN scientists hypothesized that PRRSV infection should produce a serum protein profile characteristic of early infection. They obtained a serum profile of low mw proteins in sera from PRRSV-infected and non-infected pigs by mass spectrometry. Comparative analysis revealed a protein in PRRS sera within 1 dpi, with sensitivity = 0.92 and specificity = 0.94 at 7dpi. When sera from pigs infected with non-PRRSV pathogens were included specificity = 0.83. The protein was identified as the alpha1S subunit of porcine haptoglobin (a1Hp) as confirmed by immunoblotting. The results suggest that the a1Hp, a well known acute phase protein, is a potential protein biomarker for acute PRRS, thus providing new insights into biochemical processing of Hp and its role in PRRSV pathogenesis.

2.3 Antibodies.

In previous studies NADC and Univ. IA scientists observed in gnotobiotic isolator piglets infected with PRRS virus (PRRSV) the development of lymphoid hyperplasia, hypergammaglobulinemia and autoimmunity. Preliminary characterization of the expanded B cell population in these animals reveals that gnotobiotic isolator piglets infected with PRRSV do not diversify the VDJ repertoire of their circulating B cells or that of B cells in infected tissues. This may indicate that B cells with hydrophobic HCDR3s in PRRSV-infected piglets are targeted for T cell-independent proliferation without repertoire diversification.
It has been hypothesized from gnotobiotic pig studies that polyclonal humoral responses are responsible for viral pathogenesis and establishment of persistence in PRRSV infection. UMN and ISU scientists quantified actively secreting IgG total plasma cell responses in conventional pigs by ELISPOT assay. No change in IgG total blood plasma cell responses among PRRSV infected animals, KLH immunized and uninfected animals was found, indicating that there is no non-specific polyclonal B-cell activation in conventional pigs in PRRSV infection. There is a slight elevation in serum Ig levels but that might be common in viral infections. Altogether PRRSV infection did not induce any pathological, non-specific polyclonal B-cell activation or hypergammaglobulinemia in conventionally raised pigs.

2.4 Persistent infection in pigs.

The "Big Pig" project, a multi-disciplinary, multi-institutional (KSU, ISU, SDSU, BARC, IDEXX Labs) project, monitored PRRSV infection responses of 165 pigs for as long as 203 days. BARC scientists compared RNA prepared from lung and tracheobronchial lymph nodes (TBLN). Infected pigs showed up regulation of innate and IFNG stimulated, T helper 1 (Th1) genes in the first 84 days after infection followed by overall down regulation. However, there was no pattern of TBLN cytokine expression that was associated, or might help predict, which pigs will clear virus and distinguish them from those that remain persistently infected.
UMN, KSU and ISU scientists investigated the antibody response to PRRSV GP5 and M. Little is known about the role of the GP5-M heterodimeric structure in anti-viral immunity. They hypothesized that antibodies directed to conformational epitopes on the ectodomains of GP5 and M proteins may be involved in virus neutralization. Pigs infected with PRRSV developed anti-GP5-M antibody response that was long-lasting, but neutralizing antibody titers were low at 193 dpi. There was no apparent correlation between anti-GP5-M antibody response and the serum total neutralization titers, nor to resistance to challenge. Pigs immunized with GP5-M developed high antibody response and had partial protection against challenge, but no neutralizing activity was detected. This suggests that antibodies to GP5-M may play a role in protection against PRRSV that is not dependent on viral neutralization.

2.5 Viral genome.

Guelph scientists worked to understand the pathogenic role of viral proteins during infection and their interactions with host cell proteins. They identified a specific signal responsible for nuclear translocation of the viral capsid protein, and by mutating the signal sequence, the translocation was blocked. This was the basis for constructing a genetically modified PRRSV, using an infectious cDNA clone, of which the viral capsid protein is no longer translocated in the nucleus. This newly constructed PRRSV induced higher neutralizing antibodies in pigs than wild-type PRRSV, and the clinical outcome tends to be somewhat milder. This study reveals one of the pathogenic mechanisms that PRRSV plays during infection, and shows how this process can be blocked by genetic modification of the virus.
SDSU in collaboration with KSU, UMN and UNL constructed a European-like Type 1 PRRSV full-length cDNA infectious clone (pSD 01-08) to further characterize this group of U.S. Type 1 PRRSV. This virus has low virulence in pigs and induces an early and robust neutralizing antibody response. SDSU, KSU, BARC and Boehringer Ingelheim Vetmedica Inc. (BIVI) scientists characterized the immune response to this cDNA infectious clone. In vivo studies showed similar observations form animals challenged with cloned viruses as those with the parental virus or vaccine. The full-length cDNA infectious clone derived from SD 01-08 P34 could be an ideal viral backbone for future recombinant PRRSV vaccine construction.
SDSU and KSU are using infectious clones of European-like PRRSV to determine the usefulness of nsps as potential epidemiological tools. Phylogenetic analysis using ORF5 nucleotide sequences from 6 U.S. Type 1 isolates from geographically separated swine herds showed that 15/16 isolates formed a monomorphic clade of four subgroups. Comparative analysis with the genomic sequences of Lelystad virus (LV) and North American (VR-2332) revealed that each of the European-like viral genomes had higher nucleotide homology with the LV than the VR-2332. Nsps1², 2, 6 and 12 were identified as the most variable nsp regions. Nsp2 showed similar genetic heterogeneity among isolates as GP5, which has been used most frequently for PRRSV genetic diversity and evolution studies.
At UMN numerous infectious clones have been developed for the study of mechanisms of PRRSV pathogenesis. In collaboration with BIVI, recombinant constructs were generated, characterized and forwarded to BIVI for in vivo testing. The UMN laboratory is also studying the effects of deletions made to nsp2 region of the replicase; 2 deletion mutants represent a 111 and a 200 aa deletion in nsp2. Additional constructs were generated in collaboration with Northern MI Univ. (NMI) to study the effects of N-glycosylation of GP5; 11 successfully produced intact virus. Several had a mutation at N-51, the N-glycan site critical for viral growth and are being analyzed further.
2.6. Pathogenesis (virus factors).

In a Multistate initiative, UMN, Guelph, SDSU and NMI scientists are further characterizing GP2, 3 and 4 of 3 North American PRRSV strains. They both have successfully generated plasmids that express only the ORF in question, and have begun to study its ability to produce protein in rabbit reticulocyte lysates. Eukaryotic expression is underway at UMN; proteins produced were sent to SDSU for immunization of rabbits.
UNL scientists verified that certain PRRSV nsps and two structural genes, GP5 and GP2, are heavily involved in virulence. Since GP5 does actually interact with the cell receptor, attention switched to GP2, now shown to be associated with virulence. PRRSV evades the immune system by means of a glycan-shielding mechanism; the deglycosylation of the PRRSV GP5 enhances PRRSV protective antibody response. These concepts, will be used to differentiate vaccinated pigs from infected pigs (DIVA). This is a major target for PRRSV vaccinology. A reverse genetics experimental system for PRRSV has been established at UNL and is being used by labs worldwide.
Efforts at VA Tech have been aimed at developing novel antivirals against PRRSV by suppressing PRRSV replication using a novel class of antisense compounds, testing their ability to suppress PRRSV replication in cell culture. Of six tested, one (5UP1) was found to be highly effective at reducing PRRSV replication, generating up to 4.5log reduction in infectious viral titer, as confirmed by immunofluorescence assay. Production of PRRSV negative-sense RNA was reduced if 5UP1 was added to cells at up to 6hpi. These results indicate that 5UP1 has potential as an anti-PRRSV agent.
2.7. Pathogenesis (host factors).

Understanding the effects of PRRSV infection on expression of host genes will provide targets for pharmacologic and genetic interventions to control infection. Serial analysis of gene expression (SAGE) has the ability to quantify expression of all genes within a population of cells. MARC and NADC scientists have initiated the development of SAGE libraries from PRRSV-infected PAMs. These libraries will be available to researchers; a feature of SAGE is that rare gene transcripts may be detected simply by sequencing more clones from the libraries.
UIUC scientists asked whether cell-mediated immunity (CMI) against PRRSV virus is correlated with protection against reproductive failure in sows during clinical outbreaks of PRRS in 4 commercial breeding herds. A negative association between the intensity of the CMI response and the number of pigs born dead per litter was detected on 1 farm. Evidence that a strong CMI response was correlated with protection against clinical PRRS was detected in 3 of 4 farms. However, farms and sows within farms varied considerably in their immune responsiveness and in the degree to which they were protected clinically.
A UIUC longitudinal prospective cohort study was designed to compare the reproductive performance of randomly assigned pigs inoculated with a farm strain of PRRSV to that of naturally infected pigs on an operational US swine farm. Cohort-1 consisted of pigs exposed to an attenuated farm strain of PRRSV and maintained in isolation. Cohort-2 were contact exposed by cohabitation with cohort-1 pigs. Cohort-3 were pigs co-mingled with pigs of cohorts 1 and 2 when all were moved into a grow-finish facility at 8 wks age (delayed contact exposure). Viral RNA could not be detected in tonsil of any pig pre-breeding. At 17 wks age (half way between entry into grower finisher and pre-breeding), the ELISPOT responses were 96 ± 48, 97 ± 54, and 83 ± 49 respectively. The total number of piglets weaned averaged 9.9 ± 2.8, 8.9 ± 3.6 and 9.7 ± 3.3 in cohorts 1, 2, and 3 respectively.

2.8. Host Genetic resistance

With UNL collaborators BARC scientists performed immune gene and protein expression analyses to study the genetics of PRRS resistance/susceptibility. Principal component analyses ranked 200 PRRSV infected pigs from two genetic sources for phenotypic response to PRRSV. Low PRRSV burden pigs had high weight gain, low viremia, and few lung lesions. Resistant, low PRRS burden pigs had a quicker immune response to PRRSV, low expression of IFNg in cDNA and in serum, and low serum antibodies. High pre-infection serum levels of the innate cytokine, IL-8, were also significantly associated with PRRS virus-resistance, possibly implicating activation of the innate immune system as a step to prevent viral expansion.

2.9. Vaccines / Vaccination. Scientists at VA Tech developed a unique procedure to infect pigs with infectious cDNA clone-based RNA transcripts. Direct inoculation of RNA transcripts from PRRSV infectious clones into the lymph nodes and tonsils of live pigs produces active PRRSV infection in pigs. This unique system should help scientists to directly test the effects of genetic manipulations on virus pathogenesis and replication in vivo without having to propagate the virus in cell cultures.
Development of Edible Vaccines against PRRSV has been pursued by VA Tech and ISU scientists. Preliminary work has been undertaken to create lines of transgenic maize suitable for use as an edible vaccine for PRRSV. A codon optimized ORF 5 sequence for protein production in maize was designed from cDNA of U.S. isolate ATCC VR 2385. Maize callus was transformed and recombinant GP5 identified in extracts by Western Blot. The long-term goal to help eliminate the PRRS virus from swine herds by developing transgenic plants expressing PRRSV immunogens.
Vaccines that can differentiate infected from vaccinated animals (DIVA) are a new development in PRRS vaccine design. Using reverse genetics and a PRRSV infectious cDNA clone, KSU scientists constructed a viable PRRS virus that contained a 132 amino acid deletion in nsp2, in a region that is relatively conserved and immunogenic. The deleted nsp2 peptide was recognized by sera from pigs infected with wild-type, but not recombinant viruses. The results from this study can be directly applied to the development of tagged MLV vaccines that can 1) identify vaccinated pigs, 2) distinguish vaccinated from naturally infected pigs, and 3) detect the loss of immune protection following vaccination. ISU scientists attempted to apply a DIVA concept to PRRS serology using a vaccine-virus specific antigen.
The effect of PCV2 infection on the efficacy of MLV PRRSV vaccination was assessed by VA Tech and ISU researchers. PCV2-infected, PRRSV-vaccinated, and PRRSV-challenged pigs had significantly more-severe macroscopic lung lesions pigs that were not exposed to PCV2 prior to PRRSV vaccination. Non-vaccinated PRRSV-infected pigs had a higher incidence of PRRSV antigen in lungs than did all other groups except the group infected with PCV2 prior to PRRSV. The non-vaccinated PRRSV-challenged group and the group challenged with PCV2 prior to PRRSV had lower average daily weight gain than control and vaccinated groups. This work suggests that PCV2 infection has an adverse effect on the development of protective immunity induced by PRRSV vaccine.

Objective 3. Achieve biosecurity among herds by preventing viral spread between sites.

3.1 Virus Diversity.

UMN scientists developed a High Throughput TaqMan RT-PCR for Simultaneous Detection of Type 1 and 2 PRRSV. The new format allows diagnosis of several hundred isolates per day and can also be run as a strain differentiation assay. With the emergence of new strains of PRRSV and demand for increased sensitivity, they are continually updating the test to meet the demands of veterinarians and producers.
European-like Type 1 PRRSV, known as North American (NA) Type 1 PRRSV, appeared in US swine herds in 1999. Their diversity and evolution were studied by SDSU and KSU scientists by constructing phylogenetic trees using nsp2 and ORF5 of 20 US Type 1 isolates. All but two isolates possessed a unique 51 nt deletion in nsp2, suggesting a clonal origin. Viruses could be placed into distinct groups; however, the forces driving genetic separation are complex. Incongruity between the nsp2 and ORF5 trees, identified recombination in one isolate.
ISU researchers assessed recombination events among field isolates and its impact on PRRSV molecular diagnostics and studied phenotypic and genetic difference between wild-type and attenuated PRRSV isolates. They assessed the effects of genetic variation on cross neutralization among PRRS viruses. They are examining the immunobiological significance of genetic variation among PRRS viruses to determine the correlation between genetic divergence and cross-neutralization (both in vitro and in vivo). The goal is to identify a single genetic marker on viral genes that predicts whether immune responses would be cross protective between viruses.
The N-terminal of PRRSV nsp2 encodes a putative cysteine protease (CP) responsible for nsp2/3 cleavage and predicted to function as a co-factor with the nsp4 serine protease to process the other nsp cleavage products. Using a reverse genetic system, SDSU scientists deleted immunogenic epitopes on nsp2 of a Type 1 PRRSV. All epitope deletion mutants were viable except for a mutant containing a deleted ES2 epitope located in the CP domain. Antibody responses to the CP domain were evaluated and results suggest the PRRSV nsp2 CP not only plays a key role in virus replication but may also be involved in modulation of host immunity.

3.2. Immunity and/or Cross Protection

Compared to other viruses that infect the respiratory system, PRRSV appears to induce only modest levels of IFNa. For this study by ARS NADC and PIADC scientists, pigs were injected with a non-replicating adenovirus vector expressing porcine IFNa (AdIFNa). Pigs were inoculated with AdIFNa, or adenovirus that does not express IFNa (Adnull), and challenged with PRRSV 1 day later. IFNa levels in all AdIFNa inoculated pigs were elevated the day of challenge (1 dpi) but were undetectable by 3dpi in unchallenged pigs. AdIFNa pigs had lower clinical responses, at 10dpi, delayed viremia and antibody response, and higher serum IFNa levels as a result of PRRSV infection, as compared to other pigs. Thus IFNa can have protective effects if present during the time of infection with PRRSV.

3.3. Transmission.

Understanding the dynamics of PRRSV infection within the host and at the herd level is essential for designing monitoring protocols. UMN scientists developed a Monte Carlo model that simulates the introduction and transmission of PRRSV into a negative herd (boar studs), including the changes in infection, shedding, and serology status in each boar over time. They compared different testing protocols based on frequency of sampling, type of test, individual testing or pooling.
PRRSV makes a small membrane protein, termed E protein, which when knocked-out in an infectious cDNA clone was replication-defective. Studies by Guelph researchers showed that E protein is an ion-channel protein, which is the key function for virus uncoating and subsequent multiplication in infected cells. Since the blocking of E protein function prevents PRRSV infection, a specific drug that binds to the E protein will be explored as a specific antiviral drug for PRRSV. A similar category of antiviral drugs have been developed for influenza virus in humans.

3.4. PRRS Risk Factors.

Before large-scale PRRS eradication programs can begin, a clear understanding of how PRRSV is transmitted between farms and how to prevent virus entry to naïve farms is critical. UMN investigators found that the greater the distance between farms, the less genetic homology between the PRRSV isolates. In partnership with NPB, ISU researchers have started to characterize the physical and environmental components that affect the rate of pig-to-pig PRRSV transmission within swine herds.

Objective 4. Improve diagnostic assays and create on-farm monitoring systems.

Monitoring of boar studs for PRRS is critical to minimize the risk of transmission to sows via contaminated semen. However, current protocols for monitoring PRRSV in boar studs are diverse, sometimes very costly, and their effectiveness has not been examined quantitatively. Studies conducted by SDSU and UMN evaluated 29 naïve boars inoculated with PRRSV. Results indicate that PCR using blood swabs or serum undiluted or at 1:3 or 1:5 dilutions have similar sensitivities and are useful in detecting early infection in adult boars. This study supports field observations suggesting that an intensive monitoring protocol (testing a large number of boars by PCR and at a high frequency) needs to be in place in order to detect a PRRSV introduction as early as possible.
ISU researchers investigated the use of oral fluids as a diagnostic specimen. Tests have been completed indicating the utility of ropes for stimulation of saliva production and viral load monitoring.
Investigators at UMO continue to work on nanosensor technology for a fast, penside test for PRRSV. Two methods being pursued include an optical based nanobiosensor and capillary electrophoresis on a microchip. Developing sensitive biosensors will help to quickly detect PRRSV antigen in clinical samples.
The cysteine protease domain (CP) of PRRSV nsp2 was evaluated by SDSU scientists as a potential new antigen for sensitive, specific and differential diagnostic ELISA tests since antibody to CP can detected as early as 14 dpi. The CP-based ELISA was determined with 93% agreement with the IDEXX ELISA. To differentiate Type 1 and 2 PRRSV, an epitope-based ELISA using the conserved ES2 epitope of Type 1 PRRSV was developed and showed good specificity (94.4%) and sensitivity (94.5%) for Type 1 PRRSV.

Objective 5. Develop and test PRRSV virus eradication protocols under various ecological settings.

NCSU scientists experimentally determined that stable flies do internalize infectious PRRSV by consuming viremic blood meals, however, they were unable to infect naïve pigs while obtaining their next meal by natural intra-dermal feeding. PRRSV was detectable from dissected fly gut following blood meals spiked with PRRSV and was detectable by qcRTPCR up to 96 hr post-feeding (hpf); with a linear decay from 12 to 96 hpf. However, 3 attempts failed to transmit PRRSV infection to naïve pigs; with 30 to 60 bite sites observed per pig. Similar methods were used to estimate that the non-biting house fly only consumed 1 - 5 PRRS virions/meal.
Aerosol transmission studies of PRRSV by UMN and ISU scientists demonstrated a significant association between PRRSV isolate pathogenicity and shedding/transmission via aerosols. Isolate pathogenicity did not influence the concentration of PRRSV in aerosols. Pig age and co-infection with Mycoplasma hyopneumoniae (MHYO) did not impact aerosol shedding.
Utilizing a model of a swine production region to evaluate routes of transmission of PRRSV, UMN and ISU scientists evaluated seasonal risk factors and tested the ability of various biosecurity protocols to reduce the risk of PRRSV entry into naïve populations. Preliminary observations suggest that contaminated fomites, insects and aerosols are important risk for spread of PRRSV between farms and that farms equipped with an air filtration system may reduce risk.

Objective 6. Develop educational outreach tools for disseminating information through established outreach and extension networks to producers, veterinarians, educators, and researchers.

NC229 leaders serve as CoChairs for the International PRRS Symposium in Chicago IL. The 2006 symposium had 190 registrants and 70 posters. An international Scientific Advisory Board has developed the 2007 program with 77 posters, 153 registrants to date including attendees from the U.S., Mexico, Canada, Europe and Asia. The full 2007 program and 2006 abstract book are available (http://www.prrssymposium.org/).
The North American PRRS Eradication Task Force (NAPPRSETF) was created by an NCSU scientist and is a working group of the American Association of Swine Veterinarians (AASV),. The NAPPRSETFs mission is to facilitate communication of PRRS control research results and needs between producers, veterinarians, and researchers with the ultimate goal of building producer confidence and demand for PRRSV Eradication. Each NAPPRSETF Member is tasked to form Producer  Veterinary Area Task Forces to identify problems specific to their areas and communicate the need for, or propose, research projects designed to address their regions specific problems.

Objective 7. Create an information network to ensure rapid and efficient communication of PRRSV research.

Four communication initiatives were continued: the PRRS CAP 1 website (prrs.org) was expanded; quarterly newsletter provides information about NC-229/PRRS-CAP 1 activities via email; past issues are posted at the website; conference calls among CAP1 researchers expanded plans for CAP2 renewal; and many NC229 members served on the CAP2 writing team.
ISU and KSU have participated in the movement toward an open information network through our involvement in the development of the ARM-7 database using the "BigPig" data as the original dataset to expand the database for animal disease data.