Establishment of a herd negative for porcine reproductive and respiratory syndrome virus (PRRSV) from PRRSV-positive sources
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Objective: To establish a herd negative for porcine reproductive and respiratory syndrome virus (PRRSV) from PRRSV-positive sources by management of the gilt pool and batching of pig flow. Methods: Two groups of PRRSV-positive gilts were housed in common acclimatization areas for 70 to 100 days, bred in an off-site finishing facility, and farrowed in a separate facility. Piglets weaned at 5 to 7 days of age were moved to off-site nurseries in weekly batches and mixed with cohort sentinel piglets from a PRRSV-negative herd. Each nursery batch was tested for PRRSV twice by PCR and once by ELISA. Two to five negative batches were grouped in off-site grower facilities, and tested again. Negative groups moved to a quarantine facility. Negative quarantine groups were used for stocking the PRRSV-negative herd. Results: Of the 31 batches of nursery pigs produced, three batches, born 2, 4, and 6 weeks after farrowings started, were PRRSV-positive. Six grower groups (comprising 23 nursery batches) that were PRRSV-negative after repeated testing were assembled into five groups in a quarantine facility and remained PRRSV-negative. Two grower groups were rejected. A total of 9500 pigs were produced, from which 3415 pigs were selected to stock the PRRSV-negative herd. Implications: A PRRSV-negative population was established from positive sources by managing the gilt pool and batching the pig flow, allowing for preservation of elite genetics. It appeared that PRRSV infection, indicated by lack of seroconversion in the offspring, eventually either disappeared or became inactive in the donor gilt population.A porcine reproductive and respiratory syndrome virus(PRRSV) strain isolated from visceral organs was designated as PRRSV-FS.The sequence analysis revealed that the isolated virus was a mutation strain as the Nsp2 gene existed amino acid deletion of 30 and the GP5 gene was conservative relatively.The genome of PRRSV FS strain showed 88.7%,98.8%,58.5% of nucleotide indentity with ATCC VR-22332,JN-HS,Europena Lelystad virus respectively.
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Arterivirus
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The objective of this field study was to evaluate the protocol of test and removal (T&R) for the elimination of porcine reproductive and respiratory syndrome virus (PRRSV) from 5 chronically infected breeding herds. The T&R protocol involved sampling the entire breeding herd in one day, testing sera by polymerase chain reaction and ELISA to detect previously exposed and/or infected animals, and subsequently removing them from the herd. Following completion of T&R, breeding herds were monitored for 12 consecutive months, using ELISA, for the presence of antibodies to PRRSV. In order to be classified as a PRRSV-negative herd, all samples collected over the 12-month monitoring period were required to be negative by ELISA (s/p ratio < 0.4). At the conclusion of the monitoring period, all 5 farms were PRRSV-negative, according to the defined testing criteria. Approximately 2.2% (74/3408) ELISA false positive samples were detected across all 5 farms during the monitoring period. The diagnostic cost required during the T&R protocol was approximately US $10.66 per animal tested. Limitations of the study were a lack of herds with large (> 2000 sows) breeding herd inventories, and herds with a history of PRRSV vaccination.
Arterivirus
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In this study,differential centrifugation and discontinuous sucrose density gradient centrifugation were adopted to concentrate and purify porcine reproductive respiratory and syndrome virus(PRRSV),The purified PRRSV which is treated with Trichlor_trifluorethan regard as ELISA_antigen.The indirect ELISA was sensitive and specific,and it was superior to both IPMA and IFA in detecting antibodies in the sensitive.
Differential centrifugation
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SUMMARY The xenotropic (X-tropic) mouse type C virus (MuLV) and its pseudotype of murine sarcoma virus (MSV) were inoculated into several fertilized developing Pekin duck eggs. The development of the duck embryos was substantially reduced in those receiving the X-tropic viruses compared to eggs inoculated only with tissue culture medium. Infectious virus was isolated from some of the adult animals; in others, evidence for integrated virus sequences in the tissues was noted. No specific pathology was found in the ducks that received X-tropic MuLV alone, but one duck developed multiple fibrosarcomas when inoculated at birth with the X-tropic virus pseudotype of MSV. Two ducks receiving X-tropic MuLV had signs of haematopoietic disorders. In addition, more virus-inoculated animals had evidence of hepatitis and encephalitis than control ducks. Antibody production to X-tropic MuLV was present in several ducks inoculated with virus either in embryo or at birth. Absence of antiviral antibodies was noted in those animals whose tissues contained replicating virus. These studies confirm the observations with X-tropic virus in tissue culture. They demonstrate in vivo that avian species are susceptible to infection by the mouse X-tropic virus and that their fibroblasts can be transformed by the X-tropic MuLV pseudotype of MSV.
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Newcastle Disease
Pestivirus
Heterologous
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Seroprevalence
Arterivirus
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Alveolar macrophage
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SummarySpider monkeys and chimpanzees were given a series of three injections consisting of 17D yellow fever virus, followed by living West Nile virus, followed by a third injection which consisted of formalin-inactivated Russian spring-summer virus vaccine. On the basis of neutralizing antibody responses, the limitation of viremia, or both, developing when the animals were challenged with virulent viruses, these primates were judged to be protected to a considerable extent against Japanese B encephalitis, West Nile virus, St. Louis encephalitis, Murray Valley encephalitis virus, dengue types 1, 2, 3, and 4, two antigenic types of the Russian spring-summer virus complex, and Wesselsbron virus.An isolate of West Nile virus was passed a number of times in chick embryo tissue cultures and purified by the plaque technique. The progeny of two virus plaques, in a concentration of 106 mouse intracerebral lethal doses, did not produce encephalitis in intracerebrally inoculated rhesus monkeys. These attenuated viral preparations, on the basis of intracerebral titrations in mice, had at least 1,000 times the virus concentration that was necessary to produce encephalitis with the parent type. One of these attenuated isolates still produced homologous and heterologous neutralizing antibodies comparable to those of the parent strain. The data indicate that this attenuated West Nile virus did not revert to a more virulent form after alternate intracerebral passages in rhesus monkeys and suckling mice.The TP-21 strain of the Russian spring-summer virus complex was passed a number of times in chick embryo tissue cultures and purified by the plaque technique. The progeny from one of the virus plaques, in a concentration of approximately 300,000 mouse i.c. LD50, did not produce encephalitis when inoculated intracerebrally into rhesus monkeys. When this purified virus isolate of TP-21 was substituted for the formalin-inactivated Russian spring-summer vaccine in the triple vaccination procedure, considerable protection was noted in spider monkeys challenged with four members of the Russian spring-summer group of viruses.
Viremia
Flavivirus
Attenuated vaccine
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Abstract T’Ho virus is a poorly characterized orthoflavivirus most closely related to Rocio virus and Ilheus virus, two orthoflaviviruses associated with human disease, suggesting that T’Ho virus could also be a human pathogen. The genome of T’Ho virus has been sequenced but an isolate has never been recovered, impeding its phenotypic characterization. In an attempt to generate recombinant T’Ho virus, the entire viral genome was synthesized as three overlapping DNA fragments, joined by Gibson assembly, and transfected into mosquito cells. Several cell culture passages were performed, but virus was not recovered. Subsequent experiments focused on the development of a chimeric orthoflavivirus that contains the premembrane and envelope protein genes of T’Ho virus in the genetic background of Zika virus. The chimeric virus replicated in mosquito (C6/36) and vertebrate (Vero) cells, demonstrating that the major structural glycoproteins of T’Ho virus permit entry into both cell types. The chimeric virus produced plaques in Vero cells that were significantly smaller than those produced by Zika virus. The chimeric virus can potentially be used as a surrogate diagnostic reagent in place of T’Ho virus in plaque reduction neutralization tests, allowing T’Ho virus to be considered in the differential diagnosis.
Vero cell
Zika Virus
Flavivirus
Recombinant virus
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