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At least 433 records · Page 24Linked to original sources
PubMedDate not supplied

Response of turkeys to simultaneous vaccination with hemorrhagic enteritis and Newcastle disease viruses.

The effects of single and combined vaccination of turkeys against hemorrhagic enteritis virus (HEV) and Newcastle disease virus (NDV) were investigated. Dual vaccination of turkeys with NDV-B1 and HEVp30 or marble spleen disease virus (MSDV) enhanced white mottling of the spleens and the apoptosis rate in spleen cells (P < 0.05). In addition, simultaneously vaccinated turkeys had fewer HEV-infected spleen cells at 4 days postvaccination than turkeys given HEVp30 or MSDV alone. The anti-HEV antibody response was significantly reduced at 14 days postvaccination (P < 0.05), whereas the anti-NDV antibody response was enhanced (P < 0.05) in turkeys vaccinated with HEVp30 + NDV-B1. Further, the effect of dual vaccination on macrophage function was studied. Spleen cells from NDV-B1-vaccinated turkeys were primed to produce nitric oxide (NO) after stimulation in vitro with lipopolysaccharide. Spleen cells from HEVp30- or MSDV-vaccinated turkeys did not produce NO after in vitro stimulation. In dual-vaccinated turkeys, the priming effect of NDV-B1 was reduced in comparison with single-inoculated birds.

Adenoviridae Infections↗
PubMed1994

Vaccination of chickens with a recombinant fowlpox virus containing the hemagglutinin-neuraminidase gene of Newcastle disease virus under the control of the fowlpox virus thymidine kinase promoter.

When chickens were vaccinated with a recombinant fowlpox virus (FPV) containing the Newcastle disease virus (NDV) hemagglutinin-neuraminidase (HN) cDNA under the control of the thymidine kinase (TK) promoter and inserted into the FPV TK gene, the FPV antibody response to the recombinant virus was similar to the response to vaccination with standard FPV, and the recombinant virus protected chickens against challenge with virulent FPV. While the presence of the NDV HN cDNA was demonstrated in the recombinant virus, which was stable on serial passage, expression of HN was not detected by hemagglutination, Western blot analysis or immunoprecipitation of infected cell lysate. Chickens vaccinated with the recombinant virus failed to mount an NDV hemagglutination-inhibition antibody response, and they did not resist challenge with velogenic NDV. It was concluded that the TK promoter was too weak to drive the HN gene, but that the insertion into the FPV TK gene did not reduce the immunogenicity of the virus.

Animals↗
PubMed2005

Microarray-based detection and typing of foot-and-mouth disease virus.

Foot-and-mouth disease virus (FMDV) is the most economically important veterinary pathogen because of its highly infectious nature and the devastating effects the virus has on the livestock industry. Rapid diagnostic methods are needed for detection and typing of FMDV serotypes and differentiation from other viruses causing vesicular diseases. We developed a microarray-based test that uses a FMD DNA chip containing 155 oligonucleotide probes, 35-45 base pair (bp) long, virus-common and serotype-specific, designed from the VP3-VP1-2A region of the genome. A set of two forward primers and one reverse primer were also designed to allow amplification of approximately 1100 bp of target sequences from this region. The amplified target was labelled with Alexa-Fluor 546 dye and applied to the FMD DNA chip. A total of 23 different FMDV strains representing all seven serotypes were detected and typed by the FMD DNA chip. Microarray technology offers a unique capability to identify multiple pathogens in a single chip.

Animals↗
PubMed2001

Borna disease virus and psychiatry.

Borna disease virus (BDV), a noncytolytic neurotropic nonsegmented negative-stranded RNA virus with a wide geographic distribution, infects several vertebrate animal species and causes an immune-mediated central nervous system (CNS) disease with various manifestations, depending on both host and viral factors. In animal infections, BDV can persist in the CNS and induce alterations in brain cell functions, neurodevelopmental abnormalities and behavioral disturbances. An association between BDV and psychiatric disorders (essentially schizophrenia and affective disorders) has been suggested by some serologic and molecular studies but further investigations are required to substantiate the possible contribution of this virus to the pathogenesis of these disorders.

Autistic Disorder↗
PubMed2004

2'-fluoro-2'-deoxycytidine inhibits Borna disease virus replication and spread.

Borna disease virus (BDV) causes neurological diseases in a variety of warm-blooded animal species, possibly including humans. To date, there is no effective treatment against BDV infection. Recently, we reported on the antiviral activity of 1-beta-D-arabinofuranosylcytosine (Ara-C). However, Ara-C's cytotoxic side effects are a major obstacle for its therapeutic use. Herein, we demonstrate that the nucleoside analog 2'-fluoro-2'-deoxycytidine (2'-FdC) exhibits potent antiviral activity against BDV. Importantly, 2'-FdC-associated cytotoxicity is negligible, indicating 2'-FdC as an excellent candidate for the development of antiviral therapy against BDV.

Animals↗
PubMed1992

Follicular dendritic cell-B cell interactions in virus disease. Common localization but different cell damage caused by antibody immobilized virus?

Follicular dendritic cells (FDC) are involved in the trapping and retention of antigen-antibody complexes in lymphoid follicles. This FDC immobilized antigen is thought to be involved in the generation of memory B-lymphocytes. Follicular trapping of both Aleutian disease virus and HIV particles has been demonstrated. However as far as known their affects on FDC and follicular B-cells are completely different. It is hypothesized that the trapping of (antibody-complexed) virus particles by the FDC-network may have an important role in several virus diseases.

Aleutian Mink Disease Virus↗
PubMed1986

Similarities and dissimilarities in the structure and expression of viral genomes of various virus strains immunologically related to Marek's disease virus.

Various strains immunologically related to Marek's disease virus (MDV) have been subdivided into three serotypes: serotype 1, pathogenic strains of MDV and attenuated or apathogenic variants derived from them; serotype 2, naturally occurring apathogenic strains of MDV; serotype 3, herpesvirus of turkey (HVT). The viral genome structures of these three serotypes were compared by a simple, practical method using total DNA extracted from virus-infected cells instead of viral DNA purified from virions. The restriction endonuclease-cleavage patterns of serotype 2 viral DNA were found to differ from those of either serotype 1 MDV or serotype 3. Under stringent conditions, no significant DNA homology was detected among the three serotype viruses, except in a restricted portion of these viral genomes. Northern blot hybridization experiments suggested that virus-specific polyadenylated RNA of about 2.4 kilobases was transcribed from a restricted portion showing close homology in these viruses. Southern blot hybridization under less stringent conditions revealed that regions with weak homology were distributed over most of the viral genomes of the three serotypes. Two types of virus-specific glycoproteins, gA and gB, were identified in the immunoprecipitates of the culture medium and cell lysates, respectively, of serotype 2-infected cultures with monoclonal antibodies or hyperimmune antisera cross reactive with serotype 1 MDV and serotype 3 HVT, and detected on the surface of serotype 2-infected cells by the membrane immunofluorescence test. These results indicate a close evolutionary relationship among these three viral serotypes.

Animals↗
PubMed1997

Comparison of the complete genomic sequence of the border disease virus, BD31, to other pestiviruses.

The genus Pestivirus is composed of hog cholera virus (HCV) [also known as classical swine fever virus (CSFV)], bovine viral diarrhea virus (BVDV), and border disease virus (BDV). Complete sequences have been published for HCV (or CSFV) and the two genotypes of BVDV (BVDV1 and BVDV2). In this study the complete sequence of the border disease virus (BDV), BD31, was determined. BD31 was isolated from a lamb with hairy shaker syndrome and is the BDV type virus offered by ATCC (ATCC VR-996). The genome was 12268 nucleotides long and had a single large open reading frame (ORF) beginning at nucleotide 357 and ending at nucleotide 12045. The sequence identity of the predicted amino acid sequence of BD31 and other published pestivirus sequences varied from 71% to 78%. Phylogenetic analysis of available complete genomic sequences segregated pestiviruses into two branches. One branch contained BD31 and HCV (or CSFV) isolates while the other branch contained BVDV1 and BVDV2 isolates. Pestiviruses from the same branch were similar in the length of the 5' and 3' untranslated regions (UTR). When complete genomic sequences were compared among BD31, HCV (or CSFV), BVDV1 and BVDV2, the highest sequence identity was observed in the 5' UTR. Within the ORF, the highest sequence identity was observed in the genomic region coding for the nonstructural viral polypeptide p80.

Amino Acid Sequence↗
PubMedDate not supplied

Slow virus diseases of the central nervous system.

Slow virus diseases are characterized by a long asymptomatic period, often months or years in duration, between the introduction of the infectious agent and the appearance of clinical illness. Two distinct groups cause serious degenerative diseases of the brain and spinal cord. The first to be identified are those caused by "unconventional agents," kuru and Creutzfeldt-Jakob disease. The second category, "conventional virus diseases," include SSPE (subacute sclerosing panencephalitis), PML (progressive multifocal leukoencephalopathy), progressive rubella encephalitis, and HIV encephalopathy. The universal focus on acquired immune deficiency syndrome (AIDS) has stimulated new research on slow viruses. The extreme neurological deficits, the chronic nature of these diseases, and the possible concern with infection control make patients with these diseases a challenge to nursing.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Protection of chickens against overt clinical disease and determination of viral shedding following vaccination with commercially available Newcastle disease virus vaccines upon challenge with highly virulent virus from the California 2002 exotic Newcastle disease outbreak.

During 2002-2003, exotic Newcastle disease (END) virus caused a major outbreak among commercial and backyard poultry in southern California and adjacent states. The outbreak raised concerns regarding the protective immunity of commercially available vaccines for prevention and control of this virus in poultry. We sought to determine if existing commercial live and inactivated Newcastle disease virus (NDV) vaccines could provide protection against the 2002-2003 END virus, and whether current commercial NDV-vaccination programs for broiler-breeders (BB) and broilers (Br) would protect against END-challenge. In the first experiment, birds received a single dose of either inactivated or live B1-type vaccine at 2 weeks-of-age and were challenged 2 weeks post-vaccination with a lethal dose of END. In the second experiment, a high (10(6.9)EID50/bird) or low (10(3.9)EID50/bird) dose of live B1 was applied to 8-week-old chickens, followed by lethal END challenge. In the third experiment, NDV field-vaccinated commercial BB (65 weeks-of-age) and Br (36 days-of-age) were challenged against END virus. Results indicated that both the live and inactivated vaccines protected against morbidity and mortality and significantly reduced the incidence and viral titers shed from chickens in comparison with sham controls, but did not prevent infection and virus shedding. In addition, both doses of live vaccine protected birds and significantly decreased the number of birds shedding virus. All unvaccinated control chickens challenged with END died within 6 days post-challenge (pc). Protection from disease correlated with the presence of antibody titers (determined by enzyme-linked immunosorbent assay (ELISA) or hemagglutination inhibition (HI)) at day of challenge. Commercial BB were protected from disease and exhibited low incidence and titer of challenge virus shed. In contrast, commercial Br exhibited 66% mortality and shed significantly more virus than the BB birds. These results underscore the need to develop new NDV vaccines and vaccine strategies for use during outbreak situations to protect birds from both disease and infection to reduce virus shedding.

Animals↗
PubMed1977

Detection and localization of aleutian disease virus and its antigens in vivo by immunoferritin technique.

Tissues from mink infected with aleutian disease virus were examined by the electron microscope for the presence of virus particles. Virus-like particles, measuring 22 nm in diameter, were observed in macrophages of spleen, mesenteric lymph node and in Kupffer cells in liver of mink ten to 13 days after infection. The virus-like particles were usually present in vacuoles inside the cytoplasm of macrophages and Kupffer cells and, occasionally, similar particles were observed inside the nucleus. Cells from uninfected mink did not contain such patricles. To correlate the existence of these virus-like particles with the presence of aleutian disease virus antigen in infected cells, tissues were processed for immunoferritin technique. It was found that aleutian disease virus antigen was present in vacuoles inside the cytoplasm of cells from the infected spleen, lymph node and liver, and that the location was similar to that of the 22 nm virus-like particles. In addition, some viral antigen was also detected as cytoplasmic granular material. The nuclei of some cells also contained aleutian disease virus antigen. The pattern of aleutian disease virus antigen was similar to the distribution of virus-like particles in cells of infected tissue. It is suggested that virus replication occurs inside the nucleus with subsequent accumulation of virus in the vacuoles of the cytoplasm.

Aleutian Mink Disease↗
PubMed2005

DNA vaccination with the Aleutian mink disease virus NS1 gene confers partial protection against disease.

Aleutian disease virus (ADV) causes severe losses in mink. This happens in nature as well as in farms. In spite of several attempts to provide an efficient protective protein based vaccine, experiments have failed so far. Only partial protection has been obtained. The aim of this work was to construct and test a protective DNA vaccine based on the gene encoding for the ADV non-structural protein 1 (NS1) and to test this construct as a potential vaccine candidate against ADV infection or disease. First, the vaccine construct was tested by in vitro transfection studies. NS1 protein expression was found by immunofluorescent studies and the expected size of translated protein confirmed by Western blot. Then, 18 female mink were divided into three groups: a control group, a DNA vaccinated group, and a group which received DNA vaccine plus a boost with recombinant NS1 protein in the last immunization. After virus challenge, the two DNA vaccinated groups induced higher antibody levels in the first 23 weeks of the 32 week observation period. One month after virus challenge, the most interesting finding was, that the "DNA+protein" group exhibited a significantly higher percentage of CD8+ cells, when compared to the levels in the two other groups. This, we believe, indicate a memory CTL response created by the vaccination. Most CD8+ cells were found to contain interferon gamma as measured by FACS intracellular staining. Severity of Aleutian disease was judged by quantification of plasma gammaglobulin levels and mink death statistics. The findings let us to conclude, that the two DNA vaccinated groups of mink did show milder disease characteristics, but that the vaccine effect also in this trial could only be characterized as partial.

Aleutian Mink Disease↗
PubMed1997

A recombinant canarypox virus protects rabbits against a lethal rabbit hemorrhagic disease virus (RHDV) challenge.

An ALVAC (canarypox)-based recombinant virus ALVAC-RHDV (vCP309) expressing a native rabbit hemorrhagic disease virus (RHDV) capsid protein was derived and assessed for its protective efficacy in rabbits. Protection against a lethal RHDV challenge was demonstrated in rabbits inoculated twice with either high (10(7) p.f.u.) or low (10(5) p.f.u.) doses of vCP309. However, animals in the high dose group developed significantly higher antibody response. These results have implications that are relevant to the development of a safe rabbit hemorrhagic disease (RHD) vaccine and further illustrate the utility of the ALVAC vector system to elicit protective immune responses in nonavian species.

Animals↗