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At least 451 records · Page 25Linked to original sources
PubMed1990

Restriction fragment pattern analysis of genomes from French isolates of suis herpes virus 1 (Aujeszky's disease virus).

Purified DNA from 45 isolates of suis herpes virus 1 (SHV1) collected between 1980 and 1987 from clinical outbreaks of Aujeszky's disease on French farms was compared by restriction fragment pattern (RFP) analysis. The BamHI generated RFPs were found to be distinguishable, confirming RFP analysis as a potential epidemiological tool. The RFP could be assigned to two established major electrophoretic types and different subtypes. The RFP analysis indicated that the majority of outbreaks were caused by ADV with a central European genome type. The heterogeneity of RFPs among PRV isolates recovered from the central nervous system, lung, and foetus was not restricted specifically to one clinical entity. Variations in the virulence of the 45 isolates studied in mice, chicks, or piglets were unrelated to the RFP subtypes. One unusual RFP has been described for one strain of low virulence.

Analysis of Variance↗
PubMed2002

Molecular indications for in vivo integration of the avian leukosis virus, subgroup J-long terminal repeat into the Marek's disease virus in experimentally dually-infected chickens.

Marek's disease virus, a herpesvirus, and avian leukosis virus, subgroup J, a retrovirus, are oncogenic viruses of poultry. Both viruses may infect the same flock, the same bird and the same cell. In a double-infected cell, the retroviral DNA can integrate into the cellular or the Marek's disease virus (MDV) genome. The retroviral-long terminal repeat (LTR) integration into MDV was first described by Isfort et al., (Proc Natl Acad Sci 89, 991-995, 1992) following tissue culture co-infection. The recombinant virus isolated, RM1, had altered biological properties compared to the parental MDV (Witter R.L., Li D., Jones D., and Kung H.-J., Avian Dis 41, 407-421, 1997) . The issue of retroviral sequence integration into herpesviruses in vivo, in cases of double-virus infection is of wide significance in general virology and veterinary medicine; it also represents a special case of gene transposition. Using the avian system, we aimed to determine occurrence of such integrations in vivo. Chickens were experimentally co-infected with both avian leukosis virus (ALV) subgroup J and with MDV. To demonstrate the presence of the retroviral LTR in the MDV genome we applied the Hot Spot-combined PCR assay (Borenshtain R. and Davidson I., J Virol Meth 82, 119-127, 1999) that consisted of two consecutive steps of amplification. By that HS-cPCR assay, certain MDV genomic sites, defined as HS for integration were specifically amplified, the HS step, and then subjected to screening in an attempt to detect LTR inserts. The screening was achieved by amplification using heterologous primer sets, one for the MDV hot spot and the other for the retroviral LTR, the cPCR step. The products were Southern blotted and hybridized with MDV and ALV-LTR probes. Chimeric molecules were detected and evidenced by an intense signal in 3/10 chickens and weakly in other 3/10 birds. Detection was by LTR amplification, sequencing and multiple alignment to the ALV-J-LTR sequence. The present study indicated that chimeric molecules were produced in vivo.

Animals↗
PubMed2006

[Isolation, identification and genome sequenceing of a rabbit hemorrhagic disease virus strain WHNRH].

The rabbit hemorrhagic disease virus (RHDV) is a single-stranded positive-sense RNA virus of the family Caliciviridae with a high morbidity and mortality rates of about 90% in adult rabbits. A strain of rabbit hemorrhagic disease virus named WHNRH was isolated and identified in the research. The genome of WHNRH was then sequenced. Primers were designed referring to the genome sequences of RHDV published in GenBank and a RACE was applied to get the 5' terminus sequences. The other terminus sequences of WHNRH was acquired referring to the genome's polyA structure of RHDV. The genome was amplified with RT-PCR. All the RT-PCR products were cloned into the pMD18-T vector and sequenced. The sequencing result indicated that the complete genome of RHDV isolated strain WHNRH was composed of 7437nt (not including polyA of 3' terminus), the identities were between 89.4% and 97.1% compared with the published genome sequences of six RHDV strains. The ORF1 of the genome of WHNRH was between 10nt and 7044nt and a polypeptide with 2344 amino acids was coded, the identities of nucleotide and amino acids sequences were 89.1% - 96.1% and 96.0% - 98.4% respectively compared with the six published RHDV strains. The ORF2 of the genome of WHNRH was between 7025nt and 7378nt and a polypeptide with 177 amino acids was coded, the identities of nucleotide and amino acids sequences were all between 92.1% and 96.9% compared with the six published RHDV strains.

Animals↗
PubMed1980

Transcriptional map for Newcastle disease virus.

A transcriptional map of Newcastle disease virus was determined by measuring the kinetics of UV inactivation of the transcription of individual genes and of viral infectivity. The inactivation of single genes was monitored by measuring the reduction in the accumulation of viral gene products in vivo and in vitro. In vivo, the accumulation of viral polypeptides in infected cells was measured after reversal of a cycloheximide treatment designed to inhibit secondary transcription. Actinomycin D and a hypertonic medium were used to decrease selectively the synthesis of host cell polypeptides in infected cells. In vitro, mRNA's synthesized by irradiated viruses were analyzed by translation in cell-free systems under conditions in which the amount of each polypeptide synthesized reflected the relative abundance of the corresponding mRNA. UV target sizes were obtained for the genes coding for the HN, F0, NP, M, L, and P polypeptides; the 47,000-dalton protein was not detected. A comparison of the UV target sizes with the corresponding gene sizes suggested that transcription of these genes initiated at a single promotor and proceeded in the order NP, P, (F0, M), HN, L. These experiments were performed with Newcastle disease virus strains Australia-Victoria and B1-Hitchner; for both strains, two forms of the P polypeptide which differed in electrophoretic mobility were detected. Proof that the P protein is virus specific was obtained. In addition, infection of chicken embryo cells with avirulent strain B1-Hitchner enhanced the accumulation of at least four polypeptides that appeared to be specified by the host cell rather than by the infecting virus.

Genes, Viral↗
PubMed1998

Recombinant fowlpox viruses coexpressing chicken type I IFN and Newcastle disease virus HN and F genes: influence of IFN on protective efficacy and humoral responses of chickens following in ovo or post-hatch administration of recombinant viruses.

We have constructed recombinant (r) fowl pox viruses (FPVs) coexpressing chicken type I interferon (IFN) and/or hemagglutinin-neuraminidase (HN) and fusion (F) proteins of Newcastle disease virus (NDV). We administered rFPVs and FPV into embryonated chicken eggs at 17 days of embryonation or in chickens after hatch. Administration of FPV or rFPVs did not influence hatchability and survival of hatched chicks. In ovo or after hatch vaccination of chickens with the recombinant viruses resulted in protection against challenge with virulent FPV and NDV. Chickens vaccinated with FPV or FPV-NDV recombinant had significantly lower body weight 2 weeks following vaccination. This loss in body weight was not detected in chickens receiving FPV-IFN and FPV-NDV-IFN recombinants. Chickens vaccinated with FPV coexpressing IFN and NDV genes produced less antibodies against NDV in comparison with chickens vaccinated with FPV expressing NDV genes.

Animals↗
PubMed1986

Epidemic polyarthritis and Ross River virus disease.

Ross River virus is a mosquito-transmitted alphavirus indigenous to Australia, Papua New Guinea and nearby islands, which recently appeared in other western and central South Pacific islands. Human infection can be manifest by varied constitutional disturbances, rash and rheumatic symptoms, known in Australia as epidemic polyarthritis and broadly similar to certain alphavirus diseases in other regions. Although usually short-lived, the rash can persist for 5 months. Rheumatic effects involve synovial joints, tendon and ligaments, and can continue or recur in peripheral joints and tissues as long as 6 years, though gradually improving without destructive changes. At different times, the disease can closely simulate rubella and other virus diseases, Henoch-Schönlein syndrome, rheumatoid and other chronic rheumatic diseases. Diagnosis rests upon geography, specific serology and judicious interpretation of clinical and supportive laboratory data. Skin and synovial lesions are characterized by infiltration of mononuclear cells. Their pathogenesis most likely depends on the reaction of these cells with persistent foci of virus disseminated during the early viraemic phase of infection.

Arthritis, Infectious↗
PubMed1976

Survival of foot-and-mouth disease virus in cheese.

Persistence of foot-and-mouth disease virus during the manufacture of Cheddar, Mozzarella, Camembert cheese prepared from milk of cows experimentally infected with the virus was studied. Cheese samples were made on a laboratory scale with commercial lactic acid starter cultures and the microbial protease MARZYME as a coagulant. Milk was heated at different temperatures for different intervals before it was made into cheese. Food-and-mouth disease virus survived the acidic conditions of Cheddar and Camembert cheese processing but not that of Mozzarella. Foot-and-mouth disease virus survived processing but not curing for 30 days in Cheddar cheese preparaed from heated milk. However, the virus survived curing for 60 days but not for 120 days in cheese (pH 5) prepared from unheated milk. Foot-and-mouth disease virus survived in Camembert cheese (pH 5) for 21 days at 2 C but not for 35 days.

Animals↗
PubMed2001

Alternative cell lines for the propagation of lumpy skin disease virus.

In our Institute lumpy skin disease virus is grown on primary lamb testis cells for isolation, identification and vaccine production. However, the availability of lambs in Kenya has been seriously reduced over the past few years. This has led to an increase in the cost of using primary lamb testis cells. This study was undertaken to investigate other primary cell lines, which are easily available and provide an equivalent or better yield of lumpy skin disease virus. Foetal bovine muscle (FBM) cells were found to be an adequate alternative for lamb testis cells.

Animals↗
PubMed2002

1-beta-D-arabinofuranosylcytosine inhibits borna disease virus replication and spread.

Borna disease virus (BDV) is a nonsegmented, negative-strand RNA virus that causes neurological diseases in a variety of warm-blooded animal species. There is general consensus that BDV can also infect humans, being a possible zoonosis. Although the clinical consequences of human BDV infection are still controversial, experimental BDV infection is a well-described model for human neuropsychiatric diseases. To date, there is no effective treatment against BDV. In this paper, we demonstrate that the nucleoside analog 1-beta-D-arabinofuranosylcytosine (Ara-C), a known inhibitor of DNA polymerases, inhibits BDV replication. Ara-C treatment inhibited BDV RNA and protein synthesis and prevented BDV cell-to-cell spread in vitro. Replication of other negative-strand RNA viruses such as influenza virus or measles virus was not inhibited by Ara-C, underscoring the particularity of the replication machinery of BDV. Strikingly, Ara-C treatment induced nuclear retention of viral ribonucleoparticles. These findings could not be attributed to known effects of Ara-C on the host cell, suggesting that Ara-C directly inhibits the BDV polymerase. Finally, we show that Ara-C inhibits BDV replication in vivo in the brain of infected rats, preventing persistent infection of the central nervous system as well as the development of clinical disease. These findings open the way to the development of effective antiviral therapy against BDV.

Animals↗
PubMed1978

Behavior alterations in tree shrews (Tupaia glis, Diard 1820) induced by Borna disease virus.

Intracerebral injection of Borna disease virus in tree shrews led to a persistent infection that sometimes resulted in clinical symptoms and/or specific alterations in the animals' behavior. Whereas infective virus in the brain and in the serum antibodies were always present after infection, only some of the animals showed signs of clinical disease and behavior changes. Animals kept in pairs showed especially obvious behavior alterations expressed as an exaggeration of all the components of normal social behavior. The division of the roles between males and females was seriously disturbed. The breeding behavior of females was especially impaired, although no stress factors were given and the animals were obviously in good physical condition. Some females that were maintained solitarily showed considerably exaggerated spontaneous locomotor activities (hyperactivity) 4 weeks after infection, followed by a phase of clinical neurologic symptoms (decline phase), spatial and temporal disorientation, and alterations in comfort behavior. Following a slow recovery the animals remained unusually docile and were much less timid than before infection. A recurrence of the clinical illness is possible, as shown by the occurrence of a second decline phase. All the behavior alterations can be interpreted as a disturbance in the balance of approach and avoidance. In paired animals this imbalance results in interference with normal sociosexual behavior. These alterations indicate that BD preferentially involves the limbic system, an interpretation supported by the results of neuropathologic investigations.

Animals↗
PubMed1999

Recombinant viruses expressing the foot-and-mouth disease virus capsid precursor polypeptide (P1) induce cellular but not humoral antiviral immunity and partial protection in pigs.

The importance of the induction of virus neutralizing antibodies to provide protection against foot-and-mouth disease virus (FMDV) infection is well established. However, recent studies with recombinant adenovirus expressing the precursor polypeptide of the viral capsid (P1) indicate that cattle inoculated with this recombinant vector developed partial protection against FMDV infection, in the absence of a detectable specific humoral response. Other viral vectors have been widely used to induce protective immunity against many pathogens, and it has been reported that the use of different vectors for priming and boosting injections can provide a synergistic effect on this response. In this work, we determined the immunogenicity of two recombinant viruses (adenovirus and vaccinia) expressing P1-FMDV, administered either individually or sequentially, and the protection that they induced against FMDV challenge in pigs. A double immunization with the adeno-P1 virus was the most effective strategy at inducing protective immunity. In contrast to previous reports, the use of two different vectors for priming and boosting did not show a synergistic effect on the protection induced against FMD. Interestingly, immunized pigs developed FMDV-specific T cell responses but not detectable antibodies. Thus, the protection observed was likely to be mediated by a cellular immune response.

Animals↗
PubMed2005

Interference between mild and pathogenic strains of infectious bursal disease virus in chickens.

Infectious bursal disease virus is a contagious, immunosuppressive disease of young chickens that is controlled by vaccination. Cross-protection occurs between different strains of the virus as a result of shared neutralizing epitopes. However, interactions between two antigenically similar strains (a mild and a pathogenic) coinfecting the same host have not been investigated. Groups of specific-pathogen-free chickens were inoculated with a mild strain followed by a pathogenic strain at 0, 16, 24, or 48 hr postinoculation (PI) with a mild strain. Virus persistence and the predominant strain of the virus were determined by reverse transcriptase-polymerase chain reaction and restriction fragment length polymorphism analysis, respectively, in bursas at 2, 4, 8, 14, and 21 days PI with the pathogenic strain. Severity of infection was assessed by the bursa/body weight ratios and histopathologic lesion scores. The mild virus interfered with replication of the pathogenic virus. The greatest interference was observed when the pathogenic strain was inoculated 24 hr PI with the mild strain. The interference phenomenon observed might be due to competition for host receptor sites or production of cytokine(s). This interference phenomenon could have practical implications for vaccine usage and protection.

Animals↗
PubMed1984

[Newcastle disease virus carrier state after aerosol vaccination against the disease in chickens of various ages].

Studied was the carrier status with the Newcastle disease virus in experiments with a total of 665 birds at the age of 10 days, one month, and two months following an aerosol vaccination with a La Sota strain vaccine as well as the possibility to isolate the velogenic strain Texas GB after control infection of 10-day-old and one-month-old birds. Established was a short-term carrier status with the La Sota strain in the organs of birds up to the 6th-9th day following the aerosol vaccination. In an experiment with month-old birds originating from parental flocks immunized against Newcastle disease the La Sota virus was isolated also from the brain up to the sixth day. The resistance of birds to the infection was demonstrated at the aerosol immunization of 10-day-old and month-old- birds followed by challenging the birds with high doses of the velogenic virus strain Texas GB.

Aerosols↗
PubMed1997

Recombinant fowlpox virus vaccines against Australian virulent Marek's disease virus: gene sequence analysis and comparison of vaccine efficacy in specific pathogen free and production chickens.

We have cloned and sequenced the glycoprotein genes gB, gC and gD of the Australian virulent Marek's disease virus (MDV) isolate Woodlands No. 1. The glycoprotein gB and gC sequences were identical to the homologs of other virulent MDV type 1 strains, and the glycoprotein gD sequence contained only one unique amino acid substitution. Recombinant fowlpox viruses (rFPVs) expressing the MDV glycoprotein genes were constructed and their efficacy as vaccines was evaluated in specific pathogen free (SPF) and production chickens. Vaccination with the FPV-gB recombinant protected SPF chickens from Marek's disease mortality and tumour formation following challenge with virulent MDV Woodlands No. 1. The degree of protection from Marek's disease was dependent on the vaccine dose and route of inoculation. The rFPVs expressing gC or gD did not provide protection from Marek's disease. A rFPV expressing both gB and gC did not provide enhanced protection in comparison with the rFPV-gB alone. The rFPV-gB vaccine failed to protect commercial chickens from MD mortality and provided little protection from tumour formation in comparison with the commercial herpesvirus of turkey (HVT) vaccine. The failure to provide protection against MD may be related to the impact of maternally derived immunity to MDV and FPV and possibly the genotype of the chickens.

Amino Acid Sequence↗
PubMed2000

Antigenetically unusual Newcastle disease virus from racing pigeons in India.

Newcastle disease virus isolated from an outbreak in racing pigeons in India was found to be velogenic, based on the mean time to death in 10-day-old embryonated hen's eggs, the intravenous pathogenicity index in 6-week-old chickens and the pathogenesis in chickens and pigeons. The virus induced disease in chickens without prior adaptation in chickens. The virus was antigenically unusual since it could not be grouped with the available panel of monoclonal antibodies at the World Reference Laboratory for Newcastle disease, UK. However, commercially available lentogenic and mesogenic vaccines provided 100% protection to chickens against this antigenically unusual NDV.

Animals↗