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PubMed2006

[Construction and characterization of a recombinant fowlpox virus co-expressing F, HN genes of Newcastle disease virus and gB gene of infectious laryngnotracheitis virus].

The Fusion (F) and Haemagglutinin-Neuraminidase (HN) genes of Newcastle disease virus (NDV) and the glycoprotein B (gB) gene of infectious laryngothracheitis virus (ILTV) as well as a LacZ reporter gene were all inserted into a nonessential gene of fowlpox virus (FPV) 017 strain by homologous recombination. The NDV and ILTV genes were each under the control of a fowlpox virus immediate early/late promoter (LP2EP2) while the LacZ reporter gene expression cassette was regulated by a P11 late promoter. A recombinant FPV harboring the F, HN and gB genes as well as the LacZ gene, designated as rFPV-F/HN/gB/LacZ, was obtained after ten cycles of blue plaque purification. The presence of the NDV and ILTV genes was confirmed by PCR. The expression of the recombinant proteins in rFPV-F/HN/gB/LacZ were characterized by Western blot (F and gB proteins) and indirect immunofluorescence test (F, HN and gB proteins). The results demonstrated that all four foreign proteins, which were encoded within a 10 kb gene fragment, could be expressed authentically and efficiently. Compared to the parental virus, rFPV-F/HN/gB/LacZ showed no obvious difference with respect to virus replication and cytopathogenic effects in chicken embryo fibroblasts (CEF) cell culture. Overall, our work suggests that FPV can be a useful live virus vector for the expression of multi- foreign genes against multiple avian pathogens.

Animals↗
PubMed1994

Syngeneic lysis of reticuloendotheliosis virus-transformed cell lines transfected with Marek's disease virus genes by virus-specific cytotoxic T cells.

Cell-mediated immune responses against Marek's disease virus (MDV) antigens were examined using reticuloendotheliosis virus (REV)-transformed cell lines of two haplotypes (B19B19 and B13B13). These cell lines were stably transfected with cloned fragments of MDV DNA resulting in the expression of the MDV-specific phosphoprotein pp38. Effector cells were obtained from P2a (B19B19) and S13 (B13B13) chickens at 7 days post inoculation with REV, oncogenic or attenuated serotype 1 MDV (JM-16/O and JM-16/A, respectively), serotype 2 MDV (SB-1), or herpesvirus of turkeys (HVT). Transfection of MDV genes did not influence the expression of Class I major histocompatibility complex antigens. The optimal effector to target cell ratio was determined to be 100:1. REV-sensitized effector cells lysed REV cell lines and REV cell lines transfected with MDV DNA in a syngeneic fashion. Effector cells from chickens inoculated with JM-16/O, JM-16/A, SB-1 or HVT lysed only the syngeneic, transfected cell lines, but not the parent REV cell lines. The percentage specific release caused by the MDV-sensitized effector cells was low, but statistically significant.

Animals↗
PubMed1992

Genetic mechanisms of antigenic variation in infectious bursal disease virus: analysis of a naturally occurring variant virus.

The major immunogenic protein VP2 from a pathogenic field isolate (variant A virus) of infectious bursal disease virus (IBDV) was cloned and sequenced to examine antigenic variations. The VP2 open reading frame consists of 1509 nucleotides and codes for a 503 amino acid protein. Overall, the VP2 amino acid sequence of the variant A virus shares 98.6% identity with VP2 genes from other published IBDV strains. However, within the central region of VP2 (amino acids 222-334) lies a highly divergent area that we have termed the variable domain. Relative to five other IBDV isolates, a total of six amino acid changes occur within the variable domain of the variant A virus. At positions 284-288, a substitution of isoleucine to threonine, a decrease in the number of Chou and Fasman beta turns, and a switch from a hydrophilic to a hydrophobic region are found only in the variant A virus. Together these changes predict a decrease in antigenicity as determined by calculation of potential antigenic sites. This suggests that only minor changes within VP2 contributed to the emergence of a variant virus that can cause disease in immunized birds.

Amino Acid Sequence↗
PubMed1995

Recent isolates of Newcastle disease virus in Australia.

Forty-five recently isolated strains of Newcastle disease virus and the V4 vaccine strain of Newcastle disease virus were used to infect experimental chickens. Neither V4 nor any of the new strains produced detectable clinical disease. All the viruses produced an antibody response and spread by contact. Some of the newly isolated viruses produced a more rapid serological response than V4 virus did. Dual or multiple infections with one of the new strains of Newcastle disease virus, infectious bronchitis virus and Escherichia coli did not enhance the pathogenicity of any of the agents.

Animals↗
PubMed2002

The putative capsid protein of the newly identified avian hepatitis E virus shares antigenic epitopes with that of swine and human hepatitis E viruses and chicken big liver and spleen disease virus.

We recently identified a novel virus, designated avian hepatitis E virus (avian HEV), from chickens with hepatitis-splenomegaly (HS) syndrome in the USA. We showed that avian HEV is genetically related to swine and human HEVs. Here we report the antigenic cross-reactivity of the putative open reading frame 2 (ORF2) capsid protein of avian HEV with those of swine and human HEVs and the Australian chicken big liver and spleen disease virus (BLSV). The region encoding the C-terminal 268 amino acid residues of avian HEV ORF2 was cloned into expression vector pRSET-C. The truncated ORF2 protein was expressed in E. coli as a fusion protein and purified by affinity chromatography. Western blot analysis revealed that the avian HEV ORF2 protein reacted with antisera against the Sar-55 strain of human HEV and with convalescent antisera against swine HEV and the US2 strain of human HEV, as well as with antiserum against BLSV. Convalescent sera from specific-pathogen-free chickens experimentally infected with avian HEV also reacted with the recombinant capsid proteins of swine HEV and Sar-55 human HEV. Antisera against the US2 human HEV also reacted with recombinant ORF2 proteins of both swine HEV and Sar-55 human HEV. The antigenic cross-reactivity of the avian HEV putative capsid protein with those of swine and human HEVs was further confirmed, for the most part, by ELISA assays. The data indicate that avian HEV shares certain antigenic epitopes in its putative capsid protein with swine and human HEVs, as well as with BLSV. The results have implications for HEV diagnosis and taxonomy.

Amino Acid Sequence↗
PubMed1991

Pig herds having a single reactor to serum antibody tests to Aujeszky's disease virus.

The introduction of Aujeszky's disease virus into a herd of pigs usually results in a rapid spread of the virus and a high percentage of pigs become seropositive. However, herd monitoring for the virus occasionally reveals a single seropositive breeding pig, referred to as a single reactor. The seropositive status of single reactors may be due to previous vaccination against Aujeszky's disease, or to exposure to a field strain of the virus, or to a false positive reaction in the serological assay. During a monitoring programme in Minnesota, 30 pig herds with single serological reactors were detected. Twenty-seven of these single reactors from 19 herds were segregated from their herds immunosuppressed with dexamethasone. Aujeszky's disease virus was isolated from four of the 27 pigs. Three of the four herds subsequently had outbreaks of Aujeszky's disease, suggesting that some single reactors were infected with Aujeszky's disease virus and had the potential to spread the virus within and between herds.

Animals↗
PubMed1971

Lipoprotein inhibitor of Newcastle disease virus from chicken lung.

A lipoprotein inhibitor of Newcastle disease virus was obtained from chicken lung tissue by means of dilute alkaline extraction procedures. The inhibitor was further purified by ammonium sulfate fractionation, isoelectric precipitation, and density gradient centrifugation. The purified lipoprotein inhibited active Newcastle disease virus hemagglutination at a concentration of 2.0 mug/ml which represented a 30-fold purification over the original extract. Infection of chicken embryo fibroblasts by Newcastle disease virus was also inhibited by the purified lipoprotein, the degree of inhibition depending upon the inhibitor-to-virus ratio. Chemical analysis of the purified inhibitor provided a composition of 72% lipid, 26% protein, and 3% carbohydrate, although some compositional variation was observed from one preparation to another. The chloroform-soluble lipids were shown to contain 40 to 50% phospholipid and 10 to 20% cholesterol; of the fatty acids recovered from the saponified lipoprotein, 39% was palmitic, 22% oleic, and 17% stearic. Careful analyses of large quantities of the inhibitor revealed a small (0.84%) but significant content of sialic acid. Removal of sialic acid from the lipoprotein by means of digestion with neuraminidase produced a sharp diminution in inhibitory properties. A delipidized form of the inhibitor was obtained by ether extraction, and this material produced a single broad band of precipitate in gel immunodiffusion tests.

Animals↗
PubMed1977

[Methods for the control of avian tumour virus diseases (author's transl)].

Methods developed in the Netherlands for the control of avian tumour virus diseases, Marek's disease and lymphoid leukosis, are discussed. Marek's disease is successfully kept under control by vaccination of all day-old chickens raised for egg production. Broilers are not vaccinated. During 1975 over 23 million chicks were vaccinated with cell-associated Marek's disease virus CVI 988 vaccines and about 3 million doses of HVT vaccine were administered, mostly in lyophilised form. The mechanism of the immunity conferred by the MD vaccines is discussed. Lymphoid leukosis was successfully controlled in three inbred lines of White Leghorn chickens and in a commercial grand parent flock of White Plymouth Rocks. The control method that can be applied to flocks in the field is based on three elements: From an infected flock hens are selected in whose eggs no lymphoid leukosis viruses can be detected in pooled extracts of groups of embryos. Only eggs from hens that demonstrably do not shed virus congenitally to their embryos are used for the production of progeny. The offspring are reared in isolation until two months of age at which time the age related resistance against tumour formation appears to be sufficiently developed. The chickens are subsequently inoculated intramuscularly with lymphoid leukosis viruses of subgroups A and B and transferred to a conventional chicken house. The inoculated birds become persistently viremic, resist intramuscular challenge infections or exposure by contact, but produce virus-negative eggs during the laying period. For lymphoid leukosis, congenital infection is considered the usual mode of virus transmission. Horizontal virus transmission becomes important when virus-free chickens, reared in isolation for two months, are exposed in field conditions without previous "vaccination". During the egg-laying period of these flocks, virus shedding was observed in a similar percentage as in flocks with congenitally infected birds.

Animals↗
PubMedDate not supplied

Pathogenicity studies of an Arkansas variant infectious bursal disease virus.

A variant infectious bursal disease virus (IBDV), IBDV-s977, was blind passaged in cell culture, plaque purified, and attenuated by serial passage at a high multiplicity of infection (MOI) in chick embryo fibroblasts (CEF). Cell culture passages of virus caused less bursal atrophy and splenomegaly than did the original isolate and retained immunogenicity; however, virus tended to persist for a longer time in the bursa and spleen of birds infected with the highest CEF passages. Antibody to both low MOI and high MOI passages of IBDV-s977 poorly neutralized virus that was isolated from bursal tissue 28 days postinfection (PI). The spleens of chickens infected with the eighteenth CEF passage were negative for virus at 3 and 7 days PI but had high titers of virus at 14 and 28 days PI. There was also more virus in the bursa of birds infected with the fifteenth and eighteenth CEF passages at 28 days PI than at 7 or 14 days PI. Defective interference (DI) was demonstrated when cell cultures were coinfected with a constant amount of low MOI virus and serial dilutions of high MOI virus. There was an increase in interference score with increased passage number in CEF, and there was more interference in virus passaged at a high MOI. There was an inverse relationship between interference score and bursal lesion score and splenomegaly at 7 days PI, indicating that DI particles may be involved in virus attenuation. There was a positive relationship between interference and viral persistence in the bursa and spleen at 28 days PI. Antiserum to s977 was shown to enhance the nonlytic replication of s977 in CEF, presumably within macrophages, providing a possible mechanism for the pathotypic variation seen in emerging strains of IBDV.

Animals↗
PubMed1975

Newcastle disease virus antigens and strain variations.

Study of antigenic differences among strains of Newcastle disease virus is complicated by the presence in most field isolates and strains of several genetically distinct plaque populations, and by differences in avidity (reactions to antibody) among Newcastle disease viruses. Kinetic neutralization tests were used to demonstrate antigenic differences among 3 plaque clones of velogenic viscerotropic Newcastle disease viruses recently isolated from 3 avian species. The 3 viruses could be distinguished on the basis of plaque structure and hemagglutinin and neuraminidase activity. Antigenic differences among these viruses distinguished them from older, well characterized Newcastle disease viruses.

Animals↗
PubMed1978

The isolation and characterisation of a Newcastle disease virus from an exotic parrot.

A newcastle disease virus was isolated from a salmon-crested cockatoo (Cacatua moluccensis) illegally introduced into Australia, Viral-characterisation and chicken-transmission studies indicated that the isolate, G5320/1, was a lentogenic pathotype. It caused a severe respiratory disease in chickens exposed oronasally at 1-day old and in chickens housed at 1 day of age with chickens infected with Newcastle disease virus. No harmful effects were detected in 5-week old chickens inoculated intravenously or oranasally with the virus.

Animals↗
PubMed1994

Structural features of the ribonucleotide reductase of Aujeszky's disease virus.

A gene construct of the Aujeszky's disease virus (ADV) genome was prepared and the DNA fragment encoding the ribonucleotide reductase was structurally characterized. We determined the entire DNA sequence of two adjacent open reading frames of the ribonucleotide reductase genes with the intergenic sequence of nine base pairs. From the sequence analysis we predict that Aujeszky's disease virus encodes a ribonucleotide reductase which comprises two polypeptides--large and small subunits, with sizes of 835 and 303 amino acids, respectively. Nucleotide and amino acid sequences of the large and small subunits of the Aujeszky's disease virus ribonucleotide reductase have been compared with that of other herpesviruses, and structural features of both proteins have been characterized.

Amino Acid Sequence↗
PubMed2003

Induction of lymphopenia and inhibition of T cell function during acute infection of swine with foot and mouth disease virus (FMDV).

Foot and mouth disease virus (FMDV) is a picornavirus that causes an acute vesicular disease of cloven-hoofed animals. This virus continues to be a threat to livestock worldwide with outbreaks causing severe economic losses. The present study shows an analysis of immune system phenotype and function during the acute phase of FMDV infection in swine. In the first days of infection, a significant lymphopenia is observed that involves all T cell subsets, CD4(+), CD8(+), and CD4(+)/CD8(+). This marked lymphopenia is not a result of active infection of PBMC with the virus. Further, the response of residual peripheral blood T cells to the mitogen, Concanavalin A (ConA) is significantly reduced and occasionally eliminated. Animals usually resolve clinical signs of disease and develop antigen specific T cell responses to the virus and recover ConA reactivity. These characteristics of acute phase infection likely play an important role in viral pathogenesis, propagation and shedding of viral particles and may be targeted as a way of improving vaccine formulations.

Animals↗
PubMed1996

Unusually high seroprevalence of Borna disease virus in clade E human immunodeficiency virus type 1-infected patients with sexually transmitted diseases in Thailand.

The seroprevalence of Borna disease virus (BDV) in human immunodeficiency virus type 1-infected individuals in Thailand was examined by using recombinant BDV p24. A high (38 to 48%) rate of seroprevalence of BDV was observed in clade E-infected patients with sexually transmitted diseases, compared with those in clade E-infected prostitutes (8.3%), pregnant women (0%), clade B-infected intravenous-drug users (0%), and human immunodeficiency virus type 1-negative blood donors (1.9%).

AIDS-Related Opportunistic Infections↗
PubMed1998

[Construction and identification of recombinant fowlpox virus for expressing haemagglutinin-neuraminidase glycoprotein of Newcastle disease virus strain F48E8].

For the construction of transfer vector pFGHN1175-1, the gene encoding haemagglutinin-neuraminidase(HN) glycoprotein of newcastle disease virus(NDV) strain F48E8 was removed from plasmid pGEMHN, and inserted into the HindIII site of insertion vector pFG1175-1, downstream of P7.5 promotor. Chicken embryo fibroblast (CEF) cell cultures which had been infected with fowlpox virus (FPV) Chinese vaccine strain 282E4 for 3-4 hours were transfected with pFGHN1175-1 plasmid DNA by liposomal transfection. Recombinant FPV with blue plaques were selected and purified 3 times in CEF cell cultures overlaid agarose containing X-gal. PCR analysis and DNA dot-blotting hybridization assay indicated that the HN gene had inserted into the FPV genomic DNA. The expression of the NDV HN gene in recombinant FPV was confirmed by indirect immunofluorescence assay with specific monoclonal antibody.

Animals↗
PubMed1977

Different pools of free myoinositol in chick-embryo cells as indicated by infection with Newcastle-disease virus.

Infection of chicken fibroblasts with Newcastle-disease virus indicates that cellular inositol is compartmented in at least two pools. Only the smaller pool is directly connected with the biosynthesis of phosphatidylinositol. Entrance of exogenous inositol into this pool is inhibited by phlorizin but not by the virus. Three hours after infection Newcastle-disease virus blocks the entrance of inositol from the small pool into one (or more) subsequent larger pool(s). About five hours after infection the virus enhances the catabolism of phosphatidylinositol in chicken cells and about seven hours after infection the permeability of the plasma membrane increases.

Animals↗
PubMed1992

Borna disease virus, a negative-strand RNA virus, transcribes in the nucleus of infected cells.

Borna disease virus, an unclassified infectious agent, causes immune-mediated neurologic disease in a wide variety of animal hosts and may be involved in pathogenesis of selected neuropsychiatric diseases in man. Initial reports suggested that Borna disease virus is a single-stranded RNA virus. We describe here a method for isolation of viral particles that has allowed definitive identification of the genome as containing a negative-polarity RNA. Further, we show that the viral mRNAs are transcribed in the nucleus.

Borna disease virus↗