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PubMed1980

[Clinical significance of virus diseases].

After introductory explanations the following topics are treated: acute respiratory diseases, virus infections of the central nervous system and virus infections of the intestine. In the last paragraph the present state of virus-diagnostic possibilities is described. From this is derived that the routine use of modern virus diagnostics brings great advantages for the clinician. The intensive construction of virological laboratories for the treatment of patients is emphasized.

Acute Disease↗
PubMed1996

Serological and molecular analysis of serotype O foot-and-mouth disease virus isolated from disease outbreaks in India during 1987-91.

Foot-and-mouth disease virus (FMDV) type O outbreaks have been reported frequently in vaccinated cattle in India. Twenty-five field isolates, recovered from outbreaks in vaccinated and unvaccinated cattle between 1987 and 1991, were analyzed in relation to the vaccine strain (R2/75) by complement fixation, serum neutralization and partial nucleotide sequencing of the VP1 gene. These sequences were compared with the viral sequences in GenEMBL database. Although the Indian type O viruses were close to the European type O1 viruses, they constituted a separate group of type O FMDVs. One of the field viruses, isolated from an outbreak in vaccinated cattle and designated as BAK/90, showed significant serological and nucleotide sequence variations from the vaccine strain. Phylogenetic analysis showed that the BAK/90 and R2/75 viruses belong to separate subgroups. The other isolates were found to be serologically related to both the BAK/90 and the vaccine strain. The BAK/90 strain gave broader antigenic coverage, showed better immunogenicity, and yielded larger amounts of 146S particles in suspension cultures as compared with R2/75. Taken together, these results favour inclusion of the BAK/90 strain in the vaccine to provide adequate protection against the field variants of type O FMDV currently circulating in India.

Amino Acid Sequence↗
PubMedDate not supplied

A comparison of the onset of protection induced by Newcastle disease virus strain B1 and a fowl poxvirus recombinant Newcastle disease vaccine to a viscerotropic velogenic Newcastle disease virus challenge.

Four-week-old specific-pathogen-free white rock chickens were immunized with either a commercial recombinant fowl poxvirus-vectored Newcastle disease vaccine (FPN) expressing the hemagglutinin-neuraminidase and fusion protein genes of Newcastle disease virus (NDV) strain B1 or live NDV B1. Vaccinates and controls were challenged by eyedrop and intranasal (E/I) route with a viscerotropic velogenic NDV at 14 days postvaccination to determine the time of clearance of challenge virus. In a subsequent experiment, chickens were challenged at 3, 6, or 10 days postvaccination to determine the onset of immunity. Chickens that received a recommended field dose (1x) or a 0.01x dose of FP-N subcutaneously (s.c.) and were seropositive by hemagglutination-inhibition test at 14 days postvaccination cleared the challenge virus by 14 days postchallenge. Clinical Newcastle disease and high challenge virus titers in tissues were seen only in seronegative FP-N 0.01x dose vaccinates and controls. In a comparison of vaccination with FP-N (1x, 10(4,9) median tissue culture infective dose) s.c., B1 (10(6) median egg infective dose [EID50]) s.c., or B1 (10(6) EID50) E/I, chickens vaccinated at 6 or 10 days before challenge with all vaccines were protected against clinical disease, but only those vaccinated with B1 E/I 10 days before challenge were protected against infection with the challenge virus. Vaccination at 3 days before challenge with B1 E/I provided early protection, but severe nervous signs developed later and reduced overall protection to 60%, whereas disease in chickens vaccinated with B1 s.c. and FP-N s.c. 3 days before challenge was similar to the challenge controls.

Animals↗
PubMed1975

Comparison of RNA polymerase associated with Newcastle disease virus and a temperature-sensitive mutant of Newcastle disease virus isolated from persistently infected L cells.

An in vitro comparison was made of the RNA polymerase activity associated with Newcastle disease virus (NDVo) and three clones of the temperature-sensitive mutant (NDVpi) isolated from persistently infected L cells. Less polymerase activity was associated with the NDVpi clones. Also, compared to NDVo, an increase in incubation temperature from 32 to 37 or 42 C resulted in a marked decrease in polymerase activity for the temperature-sensitive mutants which coincided with their inability to replicate at 42 C.

Cell-Free System↗
PubMed2006

Interaction between a live avian pneumovirus vaccine and two different Newcastle disease virus vaccines in broiler chickens with maternal antibodies to Newcastle disease virus.

Broiler chicks with maternal antibodies to Newcastle disease virus (NDV) but none to avian metapneumovirus (APV) were divided into six groups. One group was kept as an unvaccinated control group. Three of the other groups were vaccinated at 1 day old with live APV vaccine or one of two live NDV vaccines (VG/GA or HB1). The remaining two groups received the APV vaccine in combination with either of the two NDV vaccines at 1 day old. At intervals after vaccination for up to 42 days, distribution of the viruses in the tissues was monitored, together with humoral antibody responses. Few NDV isolations were made from any NDV-vaccinated chicks, probably due to the presence of NDV maternal antibodies. In both dual-vaccinated groups, APV persisted longer (up to 21 days post vaccination (d.p.v.)) than in the single vaccinates (up to 14 d.p.v.). After 14 d.p.v., antibody titres against APV in both dual-vaccinated groups remained higher than the single APV vaccinates. For NDV haemagglutination inhibition antibodies, similar titres were found in the single and dual NDV VG/GA vaccinates. However, for chickens dually vaccinated with NDV HB1 and APV, the haemagglutination inhibition titres were significantly higher at 21 and 28 d.p.v. than the single HB1 vaccinates. These differences reflect the fact that NDV haemagglutination inhibition titres may depend on the NDV vaccine used.

Animals↗
PubMed2005

Mechanism of the antiviral action of 1-beta-D-arabinofuranosylcytosine on Borna disease virus.

Borna disease virus (BDV) is a nonsegmented, negative-stranded RNA virus that causes neurological diseases in a variety of warm-blooded animal species. Recently, we showed that the nucleoside analog 1-beta-D-arabinofuranosylcytosine (Ara-C) was a potent inhibitor of BDV. This finding was surprising for an RNA virus, since Ara-C is a DNA polymerase inhibitor. Thus, we sought to better define the mechanism of action of Ara-C on BDV. Here, we show that (i) this effect is specific for an arabinoside ring carrying a cytosine base, (ii) it requires phosphorylation of the nucleotide, and (iii) it can be reversed by an excess of cytidine. Using the recently described minigenome assay for BDV, we provide evidence suggesting that Ara-C may act as a competitive inhibitor of the BDV replication complex.

Antiviral Agents↗
PubMed2005

Transcriptional response of avian cells to infection with Newcastle disease virus.

Newcastle disease virus (NDV) causes widespread disease in poultry and wild-birds throughout the world. cDNA microarray analysis was used to examine the effect of NDV infection on host cell transcription. The results show that NDV infection causes an apparent suppression of the interferon response genes during the early stages of infection. In addition, the results reveal transcriptional silencing of cytoskeletal proteins such as the alpha, beta, and gamma types of actin, and a downregulation of the thioredoxin gene, a likely mediator of apoptosis with possible implications in NDV pathogenesis. Comparative analyses show that a majority of genes that were transcriptionally regulated during infection with another common respiratory pathogen of poultry, the avian pneumovirus, remained unaltered during NDV infection, suggesting that even phylogenetically related viruses elicit unique or "signature" patterns of host transcriptional profiles during infection of host cells.

Actins↗
PubMed1996

Sequence characterization of human Borna disease virus.

Borna disease virus (BDV) causes a central nervous system disease in several vertebrate animal species, which is manifest by behavioral abnormalities. Seroepidemiologic data suggest that BDV might infect humans, possibly being associated with certain mental disorders. This is further supported by the detection of both BDV-specific antigens and RNA sequences in peripheral blood mononuclear cells (PBMCs) of psychiatric patients. For the first time the sequence characterization of human BDV is documented here. BDV was recovered by co-cultivation techniques from the PBMCs of three hospitalized psychiatric patients. BDV was unequivocally identified based on sequence identification of BDV open reading frames (ORFs) p24, p16 and p56, as well as of the predicted catalytic domain of the BDV L polymerase. Each human BDV isolate had an unique sequence, but they displayed a high degree of sequence conservation with respect of BDV isolates from naturally infected animals of different species.

Adult↗
PubMedDate not supplied

Characterization of Nigerian strains of Newcastle disease virus.

Newcastle disease virus was isolated from outbreaks of the disease in vaccinated and unvaccinated poultry flocks representing commercial and backyard farms in different parts of Nigeria. On characterization, all 12 isolates were found to be velogenic.

Animals↗
PubMed2006

Shrews as reservoir hosts of borna disease virus.

Borna disease virus (BDV) is the causative agent of severe T-cell-mediated meningoencephalitis in horses, sheep, and other animal species in central Europe. Here we report the first unequivocal detection of a BDV reservoir species, the bicolored white-toothed shrew, Crocidura leucodon, in an area in Switzerland with endemic Borna disease.

Animals↗
PubMed1998

Prevalence of antibodies to bovine viral diarrhoea virus and/or border disease virus in domestic ruminants.

A total of 62 sera collected from cattle, buffalo, sheep, goats and camels were investigated for the presence of antibodies to bovine viral diarrhoea (BVD) virus. The prevalence of neutralizing antibodies to BVD virus was 49.2, 52.0, 27.5, 31.4 and 52.5% in cattle, buffalo, sheep, goats and camels, respectively. The positive sera were titrated against BVD virus (BVDV) strains NADL and Oregon C24V; the latter is closely related to border disease (BD) virus. The frequency distributions of the antibody titres to both strains are presented. The statistical analysis shows no significant difference between the antibody titres to BVDV strains NADL and Oregon C24V in cattle, buffalo, sheep, goats and camels. On the other hand antibody titres to BVDV were significantly higher (P < 0.05) in cattle and buffalo in comparison with sheep, goats and camels. The cell-bound immunoassay (CBIA) is a serological rest established for the detection and titration of antibodies to BVD virus and BD virus. The percentage of agreement between the CBIA and the neutralizing peroxidase-linked antibody (NPLA) test was 96.1 and 95.3% in cattle and buffalo, respectively. The sensitivity of the CBIA in comparison with the NPLA was 100% while the specificity was 92.3 and 90.3% when testing the sera of cattle and buffalo, respectively. The method is easy to perform, cheap and suitable for the conditions in Egypt.

Animals↗
PubMedDate not supplied

Borna disease virus.

Borna disease virus (BDV) is unique amongst animal RNA viruses in its molecular biology and capacity to cause persistent, noncytolytic CNS-infection in a wide variety of host species. Unlike other non-segmented negative-strand RNA animal viruses, BDV replicates in the nucleus of the host cell where splicing is employed for expression of a very compact genome. Epidemiological studies indicate a broad host range and geographical distribution, and some investigators have proposed that human infection may result in neuropsychiatric disorders. Experimental Borna disease in neonatal and adult rats provides an intriguing model for immune-mediated disturbances of brain development and function.

Animals↗
PubMed1985

Analysis of Aleutian disease virus infection in vitro and in vivo: demonstration of Aleutian disease virus DNA in tissues of infected mink.

Aleutian disease virus (ADV) infection was analyzed in vivo and in vitro to compare virus replication in cell culture and in mink. Initial experiments compared cultures of Crandell feline kidney (CRFK) cells infected with the avirulent ADV-G strain or the highly virulent Utah I ADV. The number of ADV-infected cells was estimated by calculating the percentage of cells displaying ADV antigen by immunofluorescence (IFA), and several parameters of infection were determined. Infected cells contained large quantities of viral DNA (more than 10(5) genomes per infected cell) as estimated by dot-blot DNA-DNA hybridization, and much of the viral DNA, when analyzed by Southern blot hybridization, was found to be of a 4.8-kilobase-pair duplex monomeric replicative form (DM DNA). Furthermore, the cultures contained 7 to 67 fluorescence-forming units (FFU) per infected cell, and the ADV genome per FFU ratio ranged between 2 X 10(3) and 164 X 10(3). Finally, the pattern of viral antigen detected by IFA was characteristically nuclear, although cytoplasmic fluorescence was often found in the same cells. Because no difference was noted between the two virus strains when cultures containing similar numbers of infected cells were compared, it seemed that both viruses behaved similarly in infected cell culture. These data were used as a basis for the analysis of infection of mink by virulent Utah I ADV. Ten days after infection, the highest levels of viral DNA were detected in spleen (373 genomes per cell), mesenteric lymph node (MLN; 750 genomes per cell), and liver (373 genomes per cell). In marked contrast to infected CRFK cells, the predominant species of ADV DNA in all tissues was single-stranded virion DNA; however, 4.8-kilobase-pair DM DNA was found in MLN and spleen. This observation suggested that MLN and spleen were sites of virus replication, but that the DNA found in liver reflected sequestration of virus produced elsewhere. A final set of experiments examined MLN taken from nine mink 10 days after Utah I ADV infection. All of the nodes contained ADV DNA (46 to 750 genomes per cell), and although single-stranded virion DNA was always the most abundant species, DM DNA was observed. All of the lymph nodes contained virus infectious for CRFK cells, but when the genome per FFU ratio was calculated, virus from the lymph nodes required almost 1,000 times more genomes to produce an FFU than did virus prepared from infected cell cultures.(ABSTRACT TRUNCATED AT 400 WORDS)

Aleutian Mink Disease↗
PubMed2000

Isolation and characterization of a new subtype of Borna disease virus.

Borna disease virus (BDV), the causative agent of severe meningoencephalitis in a wide variety of animal species, has been considered to be genetically invariable and to form a single type within the genus Bornavirus of the family Bornaviridae. BDV infections are of particular interest, because for the first time a virus infection appears to be linked to human psychiatric disorders. We now describe a new subtype of BDV isolated from a horse which was euthanatized due to severe, incurable neurological disease. The nucleotide sequence of this new strain, named No/98, differs from the reference strains by more than 15%, and the subtype is difficult to detect by standard reverse transcriptase PCR protocols. The nucleotide exchanges of the novel BDV isolate have surprisingly little effect on the primary structures of most viral proteins, with the notable exception of the X protein (p10), which is only 81% identical to its counterpart in reference strains. Our data indicate that the genome of BDV is far more variable than previously assumed and that naturally occurring subtypes may escape detection by currently used diagnostic assays.

Animals↗
PubMed1983

Simple procedure for preparation of bluetongue virus and epizootic hemorrhagic disease virus antigens for agar gel immunodiffusion.

A simplified procedure was developed for preparing soluble antigen from two related orbiviruses, bluetongue and epizootic hemorrhagic disease viruses, for agar gel immunodiffusion. The antigens gave excellent results in both micro-agar gel diffusion (agar gel precipitin) and macro-agar gel diffusion (bluetongue immunodiffusion). Minor modification in the spatial arrangement of reference antisera, commonly utilized in the agar gel immunodiffusion tests, was employed to reduce the possible development of false-positive reactions. The procedures for antigen preparation were inexpensive and did not require elaborate filtration or high-speed centrifugation. Stability of antigen preparations at 5 degrees C was excellent (in excess of 3 years for bluetongue virus and 2 years for epizootic hemorrhagic disease virus).

Animals↗