.The establishment of an arterivirus family acknowledgesthemanyuniquebiologicalandmolecularpropertiesofitsfourpresent members. On the other hand, the aﬃliation with thecoronavirusesrecognizesanintriguingancestralrelationshipatthelevelofgenomeorganizationandreplication.ThegenomesequencesofEAV,PRRSV,LDVandSHFVwereinstrumentalin uniting and reclassifying the arteriviruses (den Boon

The molecular biology of arteriviruses.

In 1987, porcine reproductive and respiratory syndrome (PRRS) was recognized in the USA as a new disease of swine causing late-term reproductive failure and severe pneumonia in neonatal pigs. The syndrome is caused by an RNA virus referred to as PRRS virus (PRRSV), which is classified in the family Arteriviridae. Swine macrophages are the only indigenous cell type known to support PRRSV replication. Direct contact between infected and naive pigs is the predominant route of PRRSV transmission. Exposure of a mucosal surface to PRRSV leads to virus replication in regional macrophages, a prolonged viremia and systemic distribution of virus to other macrophage populations. Reproductive failure induced by PRRSV infection in late-gestation sows is characterized by premature farrowing of stillborn, partially autolyzed, and mummified fetuses. Pneumonia caused by PRRSV infection is more severe in young pigs compared to adults and may be complicated by concurrent bacterial infections. Gross lung lesions associated w...

https://journals.sagepub.com/doi/pdf/10.1177/030098589803500101

Porcine reproductive and respiratory syndrome

A recent epizootic of swine infertility and respiratory syndrome (SIRS) in a Minnesota swine herd was investigated. Examination of a sow, neonatal piglets, and stillborn fetuses obtained during the epizootic from the affected herd revealed interstitial pneumonitis, lymphomononuclear encephalitis, and lymphomononuclear myocarditis in the piglets and focal vasculitis in the brain of the sow. Fetuses did not have microscopic lesions. No cause for the infertility and respiratory syndrome was determined. Therefore, attempts were made to experimentally reproduce the disease. Eleven 3-day-old gnotobiotic piglets exposed intranasally to tissue homogenates of piglets from the epizootic became inappetent and febrile by 2-4 days postexposure and had interstitial pneumonitis and encephalitis similar to that seen in the field outbreak. After 2 blind passages in gnotobiotic piglets, tissue homogenates were cultured on continuous cell line CL2621, and a cytopathic virus (ATCC VR-2332), provisionally named SIRS virus, was isolated. Gnotobiotic piglets exposed intranasally to the SIRS virus developed clinical signs and microscopic lesions that were the same as those in piglets exposed to the tissue homogenates, and the virus was reisolated from their lungs. This is the first isolate of SIRS virus in the United States that fulfills Koch's postulates in producing the respiratory form of the disease in gnotobiotic piglets and the first report of isolation and propagation of the virus on a continuous cell line (CL2621). The virus is designated as American Type Culture Collection VR-2332.

https://journals.sagepub.com/doi/pdf/10.1177/104063879200400201

Isolation of swine infertility and respiratory syndrome virus (isolate ATCC VR-2332) in North America and experimental reproduction of the disease in gnotobiotic pigs

Porcine reproductive and respiratory syndrome virus (PRRSV) is a recently described arterivirus responsible for disease in swine worldwide. Comparative sequence analysis of 3′-terminal structural genes of the single-stranded RNA viral genome revealed the presence of two genotypic classes of PRRSV, represented by the prototype North American and European strains, VR-2332 and Lelystad virus (LV), respectively. To better understand the evolution and pathogenicity of PRRSV, we obtained the 12,066-base 5′-terminal nucleotide sequence of VR-2332, encoding the viral replication activities, and compared it to those of LV and other arteriviruses. VR-2332 and LV differ markedly in the 5′ leader and sections of the open reading frame (ORF) 1a region. The ORF 1b sequence was nearly colinear but varied in similarity of proteins encoded in identified regions. Furthermore, molecular and biochemical analysis of subgenomic mRNA (sgmRNA) processing revealed extensive variation in the number of sgmRNAs which may be generated during infection and in the lengths of noncoding sequence between leader-body junctions and the translation-initiating codon AUG. In addition, VR-2332 and LV select different leader-body junction sites from a pool of similar candidate sites to produce sgmRNA 7, encoding the viral nucleocapsid protein. The presence of substantial variations across the entire genome and in sgmRNA processing indicates that PRRSV has evolved independently on separate continents. The near-simultaneous global emergence of a new swine disease caused by divergently evolved viruses suggests that changes in swine husbandry and management may have contributed to the emergence of PRRS.

Porcine reproductive and respiratory syndrome virus comparison: divergent evolution on two continents.

One hundred 4-week-old cesarean-derived colostrum-deprived pigs were inoculated with one of two different US porcine reproductive and respiratory syndrome virus (PRRSV) isolates (VR2385, VR2431) or the European Lelystad virus to detect and compare the location and amount of virus antigen. Interstitial pneumonia, myocarditis, lymphadenopathy, and encephalitis were consistently seen in all three groups; however, disease and lesions were more severe in the VR2385 group. Immunohistochemical evaluation of formalin-fixed tissues revealed virus antigen in alveolar macrophages in lungs of 22/25, 14/25, 14/25, and 0/25 of the VR2385, VR2431, Lelystad, and control pigs, respectively. Follicular macrophages and dendritic cells in the lymph nodes of 14/25, 10/25, 10/25, and 0/25 pigs from the VR2385, VR2431, Lelystad, and control groups, respectively, stained positive for virus antigen. Similar cells in the tonsils from 25/25, 21/25, 23/25, and 0/25 pigs from the VR2385, VR2431, Lelystad, and control groups, respectively, stained positive for virus antigen. Other tissues and cells in which virus antigen was detected included macrophages and endothelial cells in the heart, macrophages, and interdigitating cells in the thymus, macrophages and dendritic cells in the spleen and Peyer's patches, and macrophages in hepatic sinusoids, renal medullary interstitium, and adrenal gland. PRRSV persisted in macrophages in the lung, tonsil, lymph node, and spleen for at least 28 days. Significantly more PRRSV antigen was detected in the lung (P < 0.01), lymph nodes (P < or = 0.05), and tonsils (P < 0.05) of the VR2385 pigs than was detected in the same tissues of the VR2431 and Lelystad pigs. The cell types in which PRRSV antigen was detected and the distribution of PRRSV antigen-positive cells within particular tissues and organs were generally similar for the different virus inoculation groups despite differences in virulence of the isolates.

https://journals.sagepub.com/doi/pdf/10.1177/030098589503200606

Comparison of the Pathogenicity of Two US Porcine Reproductive and Respiratory Syndrome Virus Isolates with that of the Lelystad Virus

The characterization of an isolate of swine infertility and respiratory syndrome (SIRS) virus (ATCC VR-2332) is reported. A commercial cell line (CL262 1) was used for the propagation of the virus for all assays. Laboratory studies indicate that this isolate is a fastidious, nonhemagglutinating, enveloped RNA virus. Cesium chloride-purified virions visualized by electron microscopy were spherical particles with an average diameter of 62 nm (range: 48–83 nm) and a 25–30 nm core surrounded by an envelope. Virus replication was restricted to the cytoplasm, as demonstrated by immunofluorescence. The virus did not react serologically with antisera to several common porcine viruses or with antisera to known viruses in the alphavirus, rubivirus, pestivirus, and ungrouped lactic dehydrogenase virus genera of the Togaviridae. However, convalescent sow sera and rabbit hyperimmune sera neutralized the SIRS virus at titers of 1:256 and 1:512, respectively. The virus was stable at 4 and −70 C, but was labile at 37 and...

https://journals.sagepub.com/doi/pdf/10.1177/104063879200400202

Lou Harris

Papers

Characterization of swine infertility and respiratory syndrome (SIRS) virus (isolate ATCC VR-2332).