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At least 397 records · Page 22Linked to original sources

PubMed2006

Protection against respiratory syncytial virus by a recombinant Newcastle disease virus vector.

Respiratory syncytial virus (RSV) is a major cause of severe lower respiratory tract disease in infants and the elderly, but no safe and effective RSV vaccine is yet available. For reasons that are not well understood, RSV is only weakly immunogenic, and reinfection occurs throughout life. This has complicated the search for an effective live attenuated viral vaccine, and past trials with inactivated virus preparations have led to enhanced immunopathology following natural infection. We have tested the hypothesis that weak stimulation of innate immunity by RSV correlates with ineffective adaptive responses by asking whether expression of the fusion glycoprotein of RSV by Newcastle disease virus (NDV) would stimulate a more robust immune response to RSV than primary RSV infection. NDV is a potent inducer of both alpha/beta interferon (IFN-alpha/beta) production and dendritic cell maturation, while RSV is not. When a recombinant NDV expressing the RSV fusion glycoprotein was administered to BALB/c mice, they were protected from RSV challenge, and this protection correlated with a robust anti-F CD8+ T-cell response. The effectiveness of this vaccine construct reflects the differential abilities of NDV and RSV to promote dendritic cell maturation and is retained even in the absence of a functional IFN-alpha/beta receptor.

Animals↗

PubMed2000

Synaptic pathology in Borna disease virus persistent infection.

Borna disease virus (BDV) infection of newborn rats leads to a persistent infection of the brain, which is associated with behavioral and neuroanatonomical abnormalities. These disorders occur in the absence of lymphoid cell infiltrates, and BDV-induced cell damage is restricted to defined brain areas. To investigate if damage to synaptic structures anteceded neuronal loss in BDV neonatally infected rats, we analyzed at different times postinfection the expression levels of growth-associated protein 43 and synaptophysin, two molecules involved in neuroplasticity processes. We found that BDV induced a progressive and marked decrease in the expression of these synaptic markers, which was followed by a significant loss of cortical neurons. Our findings suggest that BDV persistent infection interferes with neuroplasticity processes in specific cell populations. This, in turn, could affect the proper supply of growth factors and other molecules required for survival of selective neuronal populations within the cortex and limbic system structures.

Animals↗

PubMedDate not supplied

[Characteristics of 24S and 35S virus-specific RNA in cells infected with Newcastle disease virus].

The properties of 24S and 35S virus-specific RNAs of Newcastle disease virus were studied after denaturation. It was shown that 60-80% of 24S and 35SRNA consisted of agglomerates of molecules of virus-specific 18S RNA. Undissociable upon denaturation, 24S RNA contained mainly the same components as undenaturated RNA and consisted completely of sequences of virus-specifis 18S RNA. Undissociable 35S RNA contained no "heavy" heterogenous material present in the intact undenaturated RNA and 75% of it consisted os sequences of 18S virus-specific RNA. Some sequences present in undissociable 24S RNA were absent in undissociable 35S RNA. The aggregation of virus-specific na-transcripts and subsequent formation of covalent bonds between transcripts as well as possible formation of "solid" transcripts of the adjacent genes are discussed.

Newcastle disease virus↗

PubMed1981

Attempts ot activate endogenous virus expression with Marek's disease virus DNA.

Several DNAs derived from Marek's disease virus-infected cells and tissues were tested for in vitro infectivity and for the ability to activate avian endogenous type C virus. The DNA isolated from tumour tissue, peripheral blood buffy coat cells, MDV-infected tissue cultures, lymphoblastoid cell lines and feather follicle epithelium cells from MDV-infected birds elicited a negative response in transfection assays. The MDV DNAs isolated did not activate the endogenous type C virus from cell cultures derived from the C, I and M chicken lines. Activation was observed only in one experiment in the early period after transfection with MDV DNA. The treatment with DNase destroyed this MDV DNA activity, and lambda phage DNA and cell DNAs did not activate the endogenous viruses. Repeated experiments failed to confirm the early activation of endogenous viruses.

Animals↗

PubMed1996

Structural analysis of the interaction of the pyrimidine tract-binding protein with the internal ribosomal entry site of encephalomyocarditis virus and foot-and-mouth disease virus RNAs.

Initiation of translation of a subset of eukaryotic mRNAs results from internal ribosomal entry. This process is exemplified by encephalomyocarditis virus (EMCV), which contains an internal ribosomal entry site (IRES) within its 5' nontranslated region that is approximately 450-nt long and consists of a series of stem-loops designated H-L. We have previously identified a cellular 58-kDa polypeptide that binds specifically to this IRES and that is implicated in its function as the pyrimidine tract-binding protein PTB. We have now mapped PTB binding sites directly on the IRES elements of EMCV and the related foot-and-mouth disease virus (FMDV) using structure-specific enzymatic probes and base-specific chemical probes. PTB bound to six sites on the EMCV IRES: site 1 (UCUU401) is upstream of domain H, site 2 is the basal helix of domain H (nt 407-410 and 440-443), site 3 (UCUUU423) is the apical loop of domain H, site 4 is the apical helix and adjacent internal bulged loop of domain K, site 5 (CUUUA750) is the apical loop of domain K, and site 6 (CCUUU815) is downstream of domain L. PTB bound to sites on the FMDV IRES that correspond precisely to EMCV sites 3, 5, and 6. These sites have the consensus sequence CUUU and form two groups that are located near to the 5' and 3' borders of these IRES elements. Their position, and the effects of mutation of them on IRES function are consistent with PTB's role in IRES-mediated initiation being to bind to multiple sites in the IRES, thereby stabilizing a specific active conformation.

Aphthovirus↗

PubMed2006

Nonstructural protein of infectious bursal disease virus inhibits apoptosis at the early stage of virus infection.

Infectious bursal disease virus (IBDV), the causative agent of a highly contagious disease in chickens, carries a small nonstructural protein (NS). This protein has been implicated to play a role in the induction of apoptosis. In this study, we investigate the kinetics of viral replication during a single round of viral replication and examine the mechanism of IBDV-induced apoptosis. Our results show that it is caspase dependent and activates caspases 3 and 9. Nuclear factor kappa B (NF-kappaB) is also activated and is required for IBDV-induced apoptosis. The NF-kappaB inhibitor MG132 completely inhibited IBDV-induced DNA fragmentation, caspase 3 activation, and NF-kappaB activation. To study the function of the NS protein in this context, we generated the recombinant rGLS virus and an NS knockout mutant, rGLSNSdelta virus, using reverse genetics. Comparisons of the replication kinetics and markers for virally induced apoptosis indicated that the NS knockout mutant virus induces earlier and increased DNA fragmentation, caspase activity, and NF-kappaB activation. These results suggest that the NS protein has an antiapoptotic function at the early stage of virus infection.

Animals↗

PubMed2006

Restriction enzyme analysis of tissue culture-adapted velogenic Newcastle disease virus.

A velogenic Newcastle disease virus isolate typed to belong to group C1 by monoclonal antibody typing was adapted 50 times in chicken embryo fibroblast cell culture and 60 times in Vero cells. At every 10th passage the virus was characterized on the basis of mean death time, intracerebral pathogenicity indices and viral titration studies. A gradual reduction in the virulence of the virus was noted as the passage number increased. RT-PCR of a 254 bp region of the fusion gene encompassing the fusion protein cleavage site was carried out for the virulent as well as cell culture-adapted viruses at every 10th passage level. The amplicons were subsequently digested with three restriction enzymes, viz. AluI, HaeIII and PstI. It was found out that there was difference in banding patterns between the virulent and adapted viruses, indicating nucleotide substitutions in the virulent virus when it was sequentially passaged onto cell culture systems.

Animals↗

PubMed2006

Exposure of Mongolian gazelles (Procapra gutturosa) to foot and mouth disease virus.

Foot and mouth disease is a highly contagious acute viral disease that affects most ruminant and porcine species. During 2001, 33 serum samples were collected from Mongolian gazelles (Procapra gutturosa) in the Eastern Steppe of Mongolia. Samples were tested for antibodies to seven subtypes of foot-and-mouth-disease virus (FMDV). Antibodies were detected in 67% of the animals, and serologic results indicated exposure to FMDV-O. This virus was present in domestic animal populations in Mongolia from 2000 to 2002, and it is likely that the antibodies to FMDV detected in these gazelles resulted from spillover of virus from domestic animal sources.

Animals↗

PubMed2001

MEK-specific inhibitor U0126 blocks spread of Borna disease virus in cultured cells.

Borna disease virus (BDV) is a highly neurotropic virus that causes Borna disease, a virus-induced immune-mediated encephalomyelitis, in a variety of warm-blooded animals. Recent studies reported that BDV can be detected in patients with psychiatric disorders. BDV is noncytopathic, replicates in the nucleus of infected cells, and spreads intraaxonally in vivo. Upon infection of susceptible cultured cells, virus can be detected in foci. Little is known about the cellular components required for BDV replication. Here, we show that the cellular Raf/MEK/ERK signaling cascade is activated upon infection with BDV. In the presence of the MEK-specific inhibitor U0126, cells get infected with BDV; however, there is a block in virus spread to neighboring cells. The effect of the inhibitor on virus spread was still observed when the compound was added 2 h postinfection but not if treatment was initiated as late as 4 h after infection. Our results provide new insights into the BDV-host cell interaction and show that virus infection can be controlled with drugs interfering with a cellular signaling pathway. Since concentrations of the MEK inhibitor required to block BDV focus formation are not toxic for the host cells, our finding may be important with respect to antiviral drug development.

Animals↗

PubMed1980

Characterization of Aleutian disease virus as a parvovirus.

We characterized a strain of Aleutian disease virus adapted to growth in Crandall feline kidney cells at 31.8 degrees C. When purified from infected cells, Aleutian disease virus had a density in CsCl of 1.42 to 1.44 g/ml and was 24 to 26 nm in diameter. [3H]thymidine could be incorporated into the viral genome, and the viral DNA was then studied. In alkaline sucrose gradients, Aleutian disease virus DNA was a single species that cosedimented at 15.5S with single-stranded DNA from adeno-associated virus. When the DNA was analyzed on neutral sucrose gradients, a single species was again observed, which sedimented at 21S and was clearly distinct from 16S duplex adeno-associated virus DNA. A similar result was obtained even after incubation under annealing conditions, implying that the bulk of Aleutian disease virus virions contained a single non-complementary strand with a molecular weight of about 1.4 X 10(6). In addition, two major virus-associated polypeptides with molecular weights of 89,100 and 77,600 were demonstrated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of virus purified from infected cultures labeled with [35S]methionine. These data suggest that Aleutian disease virus is a nondefective parvovirus.

Aleutian Mink Disease Virus↗

PubMedDate not supplied

Determination of optimum formulation of a novel infectious bursal disease virus (IBDV) vaccine constructed by mixing bursal disease antibody with IBDV.

A novel vaccine against infectious bursal disease virus (IBDV) has been developed. The new vaccine was constructed by mixing bursal disease antibody (BDA) contained in whole antiserum with live IBDV before lyophilization. To establish various formulations of BDA and IBDV, several BDA doses between 5 units and 80 units of BDA/50 microliters were mixed with 100 EID50/50 microliters of IBDV suspension in Expt. 1; in Expt. 2, several IBDV doses between 10 EID50/50 microliters and 977 EID50/50 microliters of IBDV suspension were mixed with 24 units of BDA/50 microliters. Vaccine preparations were administered subcutaneously to the nape of 1-day-old specific-pathogen-free (SPF) chicks. Safety, potency, and immunogenicity of the different vaccine formulations were evaluated using bursal weight, bursal gross examination, and IBDV antibody titer. Some bursae were examined histologically to confirm gross examinations. Several vaccine formulations were safe and efficacious and met the safety, potency, and immunogenicity criteria. A vaccine construct of 100 EID50 mixed with 24 units of BDA was selected as the release dose. When administered at 1 day of age, the novel vaccine allows for delayed infection of the bursa until after days 6-8 of age in SPF chicks, while initiating potency and immunogenicity to an IBDV challenge. The addition of BDA to the IBDV results in a complex vaccine that allows for safer immunization in SPF birds than under administration of the vaccine virus without BDA.

Animals↗

PubMed1979

Biochemical studies with infectious bursal disease virus: comparison of some of its properties with infectious pancreatic necrosis virus.

Infectious bursal disease (IBD) virus was purified from the bursae of infected chickens. Two morphologically indistinguishable populations of virus particles were separated in sucrose gradients and possessed sedimentation coefficients of 295S and 460S. Both populations contained RNA and had identical polypeptide compositions. IBD virus banded at a density of 1.31 g/ml in CsCl and at 1.24 g/ml in sodium potassium tartrate. IBD virus contained two RNA segments with mol. wts. of 2.4X10(6) and 2.2X10(6) as estimated by polyacrylamide-agarose gel electrophoresis, but sedimented in sucrose gradients at 15S. Virus RNA was resistant to 0.1 micrograms/ml ribonuclease treatment under conditions in which ribosomal RNA was completely hydrolysed, but was sensitive to 1.0 and 10 micrograms/ml treatments. These results suggest that the RNA consists of either double-stranded or highly ordered single-stranded molecules. IBD virus contained seven polypeptides with mol. wts. in the range 97,000 to 24,000. Two polypeptides were absent in empty particles of IBD virus. IBD and infectious pancreatic necrosis (IPN) viruses were morphologically indistinguishable. IPN virus possessed a sedimentation coefficient of 440S and banded at a density of 1.32 g/ml in CsCl. In addition the electrophoretic mobilities of IBD and IPN virus RNAs were almost identical. Polyacrylamide slab gel electrophoresis showed that while the number and size of the polypeptides were different for each virus there were similarities in the overall pattern.

Animals↗

PubMed1952