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PubMed1995

Comparison of the structural protein coding sequences of the VR-2332 and Lelystad virus strains of the PRRS virus.

The 3'-portion of the genome of a U.S. isolate of the porcine reproductive and respiratory syndrome (PRRS) virus, ATCCVR-2332, was cloned and sequenced. The resultant 3358 nucleotides contain 6 open reading frames (ORFs) with homologies to ORFs 2 through 7 of the European strain of the PRRS virus and other members of the free-standing genus of arteriviruses. Both VR-2332 and the European isolate (called the Lelystad virus) have been identified as infectious agents responsible for the swine disease called PRRS. Comparative sequence analysis indicates that there are degrees of amino acid identity to the Lelystad virus open reading frames ranging from 55% in ORF 5 to 79% in ORF 6. Hydropathy profiles indicate that the ORFs of VR-2332 and Lelystad virus correspond structurally despite significant sequence differences. These results are consistent with the biological similarities but distinct serological properties of North American and European isolates of the virus.

Amino Acid Sequence↗

PubMed2003

Porcine reproductive and respiratory syndrome virus: origin hypothesis.

Porcine reproductive and respiratory syndrome is a serious swine disease that appeared suddenly in the midwestern United States and central Europe approximately 14 years ago; the disease has now spread worldwide. In North America and Europe, the syndrome is caused by two genotypes of porcine reproductive and respiratory syndrome virus (PRRSV), an arterivirus whose genomes diverge by approximately 40%. My hypothesis, which explains the origin and evolution of the two distinct PRRSV genotypes, is that a mutant of a closely related arterivirus of mice (lactate dehydrogenase-elevating virus) infected wild boars in central Europe. These wild boars functioned as intermediate hosts and spread the virus to North Carolina in imported, infected European wild boars in 1912; the virus then evolved independently on the two continents in the prevalent wild hog populations for approximately 70 years until independently entering the domestic pig population.

Amino Acid Sequence↗

PubMed1994

Presence of wild type Aujeszky's disease virus in swine identified as subclinical low-prevalent serological test reactors within qualified virus-negative herds.

Subclinical low-prevalent Aujeszky's disease (AD) serological test reactors are defined as those few swine within a qualified AD virus (ADV)-negative herd that have antibodies to wild type virus. However, clinical signs of the associated disease are not observed in these putatively infected swine or elsewhere in the herd. Twelve such animals, including 7 previously vaccinated with a genetically modified ADV, were identified in Illinois (USA) during a 2.5 year period. The humoral immune responses of the 5 nonvaccinated swine were assessed by an enhanced virus neutralization test and a radioimmunoassay. Anti-ADV antibodies were determined to be present in the serum from 4 of these swine. Attempts to isolate ADV by in vitro and in vivo inoculations of cell cultures and weanling mice, respectively, of tonsillar and trigeminal nerve ganglionic tissue preparations from each animal (vaccinated and nonvaccinated) were unsuccessful. Tonsillar and trigeminal nerve ganglionic tissues of each animal were screened for the presence of wild type and/or vaccine viral genomes by a soluble polymerase chain reaction (PCR) coupled with Southern hybridization. Unique PCR primers were used to distinguish between wild type and vaccine viral DNAs. An additional PCR procedure, which amplifies a portion of the essential and highly conserved viral gp50 gene, also was employed in an effort to detect viral genomes. Wild type viral DNA was found in the tissues from at least 5 of the vaccinated and 3 of the nonvaccinated swine. These results indicate that such animals should be considered as being infected with ADV. Further, these findings emphasize the need to develop highly specific and sensitive antemortem testing methods for accurate assessment of ADV infection in herds containing such subclinical, yet serologically positive, swine.

Animals↗

PubMed2026

Transcriptomic and Metabolomic Profiling Identifies a Core Gene-Metabolite Axis Driving African Swine Fever Virus Replication in the Soft Tick Ornithodoros lahorensis.

African swine fever virus (ASFV) causes an incurable swine disease with nearly 100% mortality, posing a catastrophic threat to global pig production. The soft tick Ornithodoros lahorensis acts as a critical biological vector that sustains persistent ASFV replication and mediates long-distance viral transmission, yet the molecular mechanisms governing ASFV-tick interplay remain poorly understood. Here, we integrated transcriptomics and metabolomics to systematically dissect molecular changes in O. lahorensis across three infection stages: Uninfected control, early infection (7 days post-infection, dpi), and late persistent infection (21 dpi). Multi-omics integration revealed that ASFV extensively remodels tick host metabolism, predominantly activating purine/pyrimidine metabolism, lipid biosynthesis, and energy metabolism. We further characterized a conserved regulatory module consisting of 12 core genes and 8 signature metabolites that collectively support ASFV genome replication and virion assembly. Three hub metabolic genes (TK1, ATP5F1B, and IMPDH) were selected for functional validation via siRNA silencing in ticks; individual gene silencing suppressed ASFV loads by 89.2%, 91.5%, and 87.8%, respectively (p < 0.001***). This work represents the first comprehensive multi-omics investigation of ASFV infection in O. lahorensis. We identified tick-specific molecular targets to block vector-mediated ASFV spread and established a standardized multi-omics analytical pipeline for tick-virus interaction research. Our findings elucidate the mechanistic basis of long-term ASFV persistence in soft ticks and deliver novel actionable clues for developing vector-targeted ASF intervention strategies.

Animals↗

PubMed2000

Inhibition of adhesion of Escherichia coli k88ac fimbria to its receptor, intestinal mucin-type glycoproteins, by a monoclonal antibody directed against a variable domain of the fimbria.

Strains of enterotoxigenic Escherichia coli that express K88 fimbriae are among the most common causes of diarrhea in young pigs. Adhesion of bacteria to receptors on intestinal epithelial cells, mediated by K88 fimbriae, is the initial step in the establishment of infection. Three antigenic variants of K88 fimbriae exist in nature: K88ab, K88ac, and K88ad. K88ac is the most prevalent and may be the only variant of significance in swine disease. Each K88 fimbrial variant is composed of multiple antigenic determinants. Some of these determinants are shared among the three variants and may be referred to as conserved epitopes, whereas others are unique to a specific variant and may be referred to as variable epitopes. In this study, monoclonal antibodies (MAbs) specific to either variable or conserved epitopes of K88ac fimbriae were produced. The specificity of each MAb was tested by enzyme-linked immunosorbent and immunoblot assays. Fab fragments were prepared from these MAbs and were tested for their ability to block the binding of K88-positive bacteria and purified fimbriae to porcine enterocyte brush border vesicles and purified K88 receptors, respectively. The purified receptors were intestinal mucin-type sialoglycoproteins (IMTGP) isolated from porcine enterocytes (A. K. Erickson, D. R. Baker, B. T. Bosworth, T. A. Casey, D. A. Benfield, and D. H. Francis, Infect. Immun. 62:5404-5410, 1994). Fab fragments prepared from MAbs specific for variable epitopes blocked the binding of bacteria to brush borders and of fimbriae to IMTGP. However, those from MAbs specific for a conserved epitope did not. These observations indicate that the receptor-binding domain of a K88ac fimbria is contained, at least in part, within the antigenically variable epitopes of that fimbria. Epitope mapping for one of the MAbs, which recognizes a linear epitope on K88ac fimbriae, indicated that this MAb binds to the region from amino acid no. 64 to no. 107 on the major subunit of K88ac fimbriae.

Adhesins, Escherichia coli↗

PubMed2006

The ORF3 protein of porcine circovirus type 2 is involved in viral pathogenesis in vivo.

Porcine circovirus type 2 (PCV2) is the primary causative agent of an emerging swine disease, postweaning multisystemic wasting syndrome. We previously showed that a novel identified protein, ORF3, was not essential for PCV2 replication in cultured PK15 cells and played a major role in virus-induced apoptosis. To evaluate the role of the ORF3 protein in viral pathogenesis in vivo, we inoculated 8-week-old BALB/c mice that have been developed for PCV2 replication with ORF3-deficient mutant PCV2 (mPCV2). By 42 days postinoculation, all of the mice inoculated with the mPCV2, as well as with wild-type PCV2 (wPCV2), had seroconverted to PCV2 capsid antibody, and the mutant induced levels of PCV2 antibodies that were higher than those of the wPCV2. The PCV2 genomic copy numbers in serum were significantly higher (P<0.05) in the wPCV2-inoculated mice than in mice inoculated with the mPCV2. Also, the wPCV2 caused microscopic lesions characterized by lymphocyte depletion with histiocytic infiltration of lymphoid organs, but the mutant virus failed to induce any obvious pathological lesions. In situ hybridization and immunohistochemical analyses also showed that larger amounts of viral DNA and antigens were detected in the lymph nodes of the wPCV2-inoculated than mPCV2-inoculated mice. Furthermore, animals of the wPCV2-inoculated group showed significant downshifts of CD8(+) T-cell subsets of peripheral blood lymphocytes compared to the control mice (P<0.05) at various time points postinoculation. Also, the proportions of the CD4(+) and CD4(+) CD8(+) cells were significantly reduced in wPCV2-inoculated mice at some time points postinoculation. In contrast, there are some reductions in the proportions of these subsets in the mutant virus-inoculated mice, but the proportions do not decrease significantly. Taken together, these results demonstrate that the ORF3 protein is also dispensable for viral replication in vivo and that it plays an important role in viral pathogenesis.

Animals↗

PubMed1968