Bovine diarrhea virus. II. END phenomenon: exaltation of Newcastle disease virus in bovine cells infected with bovine diarrhea virus.
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A recombinant fowlpox virus expressing the hemagglutinin-neuraminidase gene of Newcastle disease virus (NDV) protects chickens against challenge by NDV.
The hemagglutinin-neuraminidase (HN) gene from the Beaudette C strain of Newcastle disease virus (NDV) has been expressed in a recombinant fowlpox virus vector. The HN gene, under the control of the vaccinia p7.5 promoter, was inserted into a nonessential gene in the terminal inverted repeats of fowlpox virus. Expression was demonstrated in tissue culture, a protein of the correct size for fully glycosylated HN protein being recognized by an HN-specific monoclonal antibody on Western blots. When the recombinant fowlpox virus was inoculated into chickens by intravenous or wing-web routes, antibody which recognizes HN from purified NDV virions was produced. Protective immunity to NDV was generated in the chickens; at the highest dose of vaccine 100% of the chickens tested were protected against challenge with a virulent strain of NDV.
Animals↗
Electron and immunoelectron microscopy of rabbit haemorrhagic disease virus (RHDV).
Rabbit haemorrhagic disease virus (RHDV) had a calicivirus-like structure and a diameter of 31.5-33.0 nm. Antigenic relationship between the investigated RHDV strain and the causal agent of RHD in China was demonstrated by immunoelectron microscopy.
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Mutational analysis of the proteolytic cleavage site of glycoprotein B (gB) of Marek's disease virus.
The Marek's disease virus (MDV) glycoprotein B (gB) precursor, gp100, is proteolytically cleaved into two disulfide-linked subunits, gp60 and gp49. In the gB homologs of most other herpesviruses, a tetrapeptide, Arg-Xaa-Arg-Arg, is immediately upstream from the predicted cleavage site. We have investigated the specificity of the proteolytic cleavage in gp100 by introducing mutations within its predicted cleavage site (Arg-Leu-Arg-Arg) and expressed these mutants in recombinant fowlpox virus (FPV). The results show that all three Arg residues at the predicted cleavage site play an important role in the specific proteolytic cleavage of gp100. Furthermore, we demonstrated that the cleavage of gp100 is not necessary for transport of gB to the cell surface.
Amino Acid Sequence↗
Nucleotide sequence and characterization of the Marek's disease virus homologue of glycoprotein B of herpes simplex virus.
The Marek's disease virus (MDV) homologue of the herpes simplex virus (HSV) gene encoding glycoprotein B (gB) has been identified within BamHI fragments I3 and K3 of the 'highly oncogenic' strain RB1B of MDV. The entire nucleotide sequence of the gene has been determined and its predicted amino acid sequence shown to share gross overall structural features with the gB genes of HSV, varicella-zoster virus (VZV) and other mammalian herpesviruses. In particular, all 10 cysteine residues were conserved in MDV gB and there was extensive homology throughout the gene with VZV, HSV and pseudorabies virus except for the N and C termini. The overall percentage amino acid identity between MDV gB and gB of the alphaherpesviruses had a mean of 50% which was almost twice that between cytomegalovirus and Epstein-Barr virus. Northern blot analysis showed that the main RNA transcribed from this gene is approx. 2.7 kb in size. Antibodies raised against synthetic peptides (residues 250 to 271 and 304 to 330) allowed the identification of a family of serologically related glycoproteins of Mr 110K, 64K and 48K in extracts of MDV-infected cells using immunoblots. Furthermore, the antisera were able to differentiate between the antigens of MDV and herpesvirus of turkeys in immunoblots. Immunofluorescence tests indicated that MDV gB is associated with granules in the cytoplasm and is present at the surface of MDV-infected cells.
Amino Acid Sequence↗
The nucleic acid and proteins of epizootic haemorrhagic disease virus.
Purified epizootic haemorrhagic disease virus (EHDV) was shown to contain 10 double-stranded RNA segments and a double-layered protein capsid with 4 major and 4 minor polypeptides. The virus differed from bluetongue virus (BTV), the orbivirus prototype, in that EHDV had an additional minor polypeptide component. This component, together with the major polypeptides P2 and P5, formed the outer capsid layer of the virus. The extra polypeptide apparently stabilizes this layer since, unlike BTV, EHDV was quite stable on CsCl gradients at both pH 7,0 and 8,0. EHD virions were found to have a density of 1,36 g/microliter, while particles without the outer capsid layer were isolated and had a density of 1,40 g/microliter. Two non-capsid polypeptides, P5A and P6A, were identified in addition to the 8 capsid polypeptides. Polypeptide P5A was synthesized in excess of all the others. There was little homology between the nucleic acids of EHDV and BTV with only 5-10% cross-hybridization. No hybrid double-stranded RNA segments were identified. We found by cross-immune precipitation that the major core polypeptides of the 2 viruses (P7 and P3) have common antigenic determinants.
Antigens, Viral↗
[Thermostability of the vaccination strain of infectious bursal disease virus].
The vaccination strain of infectious bursal disease virus, multiplied in cultures of chick embryo cells, was very resistant to heat. At a temperature of 56 degrees C the infection titre of the virus (TCID50) decreased by 0.9 log10 within two hours and by 1.2 log10 within five hours, but the virus remained infective still after 24 hours. At a temperature of 37 degrees C, a slight decrease in infection titre was recorded only after two days and a decrease by 1.2 log10 was recorded within ten days. After the 21st day the virus was almost inactivated. At a temperature of about 20 degrees C the infection titre of the virus decreased linearly from the third to the twelfth weeks. The control samples kept at +4 degrees C retained their infectivity for three months and at -20 degrees C even for six months. The discussion deals with the effect of the concentration of protein and magnesium chloride in the medium on the thermostability of infectious bursal disease virus.
Animals↗
Virus-neutralizing and passively protective monoclonal antibodies to infectious bursal disease virus of chickens.
Murine monoclonal antibodies (MAbs) were produced to assist in the identification and characterization of the virus-neutralizing epitopes of infectious bursal disease virus (IBDV). Only MAbs that reacted in Western blotting with viral protein 2 (VP2) or immunoprecipitated VP2 neutralized the infectivity of the virus in cell culture and passively protected young chickens from infection. Three of the neutralizing MAbs did not react with denatured viral proteins. Additivity enzyme-linked immunosorbent assays indicated that the six virus-neutralizing MAbs recognized two spatially independent epitopes. The ability of two of the virus-neutralizing MAbs to neutralize a variant of IBDV that had escaped neutralization by all the other MAbs confirmed the existence of two distinct neutralizing epitopes. The results support the hypothesis that there are at least two non-overlapping epitopes recognized by the virus-neutralizing MAbs reported in this study, although these may still be within one conformational site on VP2 of IBDV.
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Genetic reassortment of infectious bursal disease virus in nature.
Infectious bursal disease virus (IBDV), a double-stranded RNA virus, is a member of the Birnaviridae family. Four pathotypes of IBDV, attenuated, virulent, antigenic variant, and very virulent (vvIBDV), have been identified. We isolated and characterized the genomic reassortant IBDV strain ZJ2000 from severe field outbreaks in commercial flocks. Full-length genomic sequence analysis showed that ZJ2000 is a natural genetic reassortant virus with segments A and B derived from attenuated and very virulent strains of IBDV, respectively. ZJ2000 exhibited delayed replication kinetics as compared to attenuated strains. However, ZJ2000 was pathogenic to specific pathogen free (SPF) chickens and chicken embryos. Similar to a standard virulent IBDV strain, ZJ2000 caused 26.7% mortality, 100% morbidity, and severe bursal lesions at both gross and histopathological levels. Taken together, our data provide direct evidence for genetic reassortment of IBDV in nature, which may play an important role in the evolution, virulence, and host range of IBDV. Our data also suggest that VP2 is not the sole determinant of IBDV virulence, and that the RNA-dependent RNA polymerase protein, VP1, may play an important role in IBDV virulence. The discovery of reassortant viruses in nature suggests an additional risk of using live IBDV vaccines, which could act as genetic donors for genome reassortment.
Amino Acid Substitution↗
Relationships among virus spread, cytopathogenicity, and virulence as revealed by the noncytopathic mutants of Newcastle disease virus.
We have studied protein synthesis in cultured cells infected with the six noncytopathic (nc) mutants of the Australia-Victoria strain (AV-WT) of Newcastle disease virus and their plaque-forming revertants. Virus-specific polypeptides accumulated at 30 to 63% of wild-type levels in nc mutant-infected cells and between 66 and 175% of wild-type levels in revertant-infected cells. An exception was the L polypeptide, which accumulated in nc mutant-infected cells at only 5 to 20% of the levels found in wild-type infection. The reduced accumulation of the L polypeptide did not appear to be due to increased degradation of that polypeptide. A new polypeptide (X) accumulated instead of polypeptide P in cells infected with mutants nc4 or nc16 and in virions released from them. Peptide mapping identified X as an altered form of P. A revertant of mutant nc4 (nc4S1), which forms larger hemadsorbing spots, but still does not form plaques, accumulated P instead of the X polypeptide. Thus, a lesion in P can affect virus spread without affecting cytopathogenicity. Virions of mutant nc7 and two naturally occurring avirulent strains of Newcastle disease virus (NJ LaSota and B1-Hitchner) contained polypeptides (F(7) and F(A), respectively) related to, but migrating more rapidly than, F(0) in sodium dodecyl sulfate-polyacrylamide gels. As previously reported for avirulent strains, a brief treatment of nc7 virions with trypsin converted F(7) to F and increased infectivity. Similarly, culturing nc7-infected cells in the presence of trypsin facilitated fusion from within and viral spread from cell to cell. A plaque-forming revertant of nc7 still accumulated F(7) in virions, indicating that the lesions responsible for the F(7) and noncytopathic phenotypes are genetically separable. The virulent parental strain, AV-WT, exhibited a mean embryo death time of 42 h. Both the larger-spot-forming revertant of nc4 (nc4S1) and the small-plaque-forming revertant of nc7 exhibited a decrease in mean embryo death time (increase in virulence) from 74 to 63 h. A second-step, plaque-forming revertant derived from nc4S1 (nc4S1R1) exhibited a further decrease in mean embryo death time from 63 to 44 h. The results suggest that the F(A)-F(7) and X lesions affect the ability of virus to spread from cell to cell. In addition, these lesions appear to be genetically separable from those responsible for the noncytopathic phenotype. However, both types of lesions cause an extension of mean embryo death time and, thus, may be relevant to virulence in vivo.
Animals↗
Foot-and-mouth disease virus.
Foot-and-mouth disease virus (FMDV) is an aphthovirus of the family Picornaviridae and the etiological agent of the economically most important animal disease. As a typical picornavirus, FMD virions are nonenveloped particles of icosahedral symmetry and its genome is a single stranded RNA of about 8500 nucleotides and of positive polarity. FMDV RNA is infectious and it replicates via a complementary, minus strand RNA. FMDV RNA replication is error-prone so that viral populations consist of mutant spectra (quasispecies) rather than a defined genomic sequence. Therefore FMDV in nature is genetically and antigenically diverse. This poses important challenges for the diagnosis, prevention and control of FMD. A deeper understanding of FMDV population complexity and evolution has suggested requirements for a new generation of anti-FMD vaccines. This is relevant to the current debate on the adequacy of non-vaccination versus vaccination policies for the control of FMD.
Animals↗
Immunogenic activity of viral polypeptides of an Indian isolate of infectious bursal disease virus.
An Indian isolate of infectious bursal disease virus, i.e. IBDV-P/AD/81, was analysed for immunogenic activity of its structural polypeptides. Virus was purified from infected bursal homogenate by sucrose density gradient centrifugation. It showed five different structural polypeptides of 75.8, 45, 40.7, 33.1 and 27 kDa molecular weights in sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE). Anti infectious bursal disease virus (IBDV) antibodies were tested using enzyme-linked immunosorbent assay (ELISA) and neutralization test (NT). Polypeptide 40.7 kDa (VP2) was known to have neutralizing epitopes. However, polyclonal anti VP2 failed to neutralize the virus. It was interpreted that VP2 had labile neutralizing epitopes which get altered confirmationally by SDS. Surprisingly, polyclonal anti 33.1 kDa (VP3) had mild neutralizing activity.
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Characterisation of New Zealand isolates of infectious bursal disease virus.
Isolates of infectious bursal disease virus (IBDV) were obtained from domestic poultry in New Zealand in 1997 and 1998. An in-vivo pathogenicity study carried out in specific pathogen free (SPF) chickens demonstrated the low virulence of one of the virus isolates. The nucleotide sequences of the hypervariable region of the VP2 gene of two isolates were determined and compared with published sequences of strains from other countries. The deduced amino acid sequence of the two New Zealand IBDV isolates showed 100% identity with each other, suggesting that little genetic drift had occurred. Phylogenetic analysis showed that the New Zealand isolates were more closely related to two attenuated IBDV strains (Cu1 and PBG98) than to classical (STC and 52/70), very virulent (DV86), variant (variant E) or Australian (002-73) strains. The results support the hypothesis that an attenuated strain of the virus was inadvertently introduced into the NZ poultry population in 1993.
Amino Acid Sequence↗
Failure of function of the "early protein" induced by an influenza virus in cells infected by Newcastle disease virus.
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Animals↗
Stimulating effect of mouse sarcoma virus on the multiplication of Newcastle disease virus.
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Animals↗
Identification of field isolates of infectious bronchitis virus by interference with the La Sota of strain of Newcastle disease virus.
The interference phenomenon of infectious bronchitis virus (IBV) with growth of Newcastle disease virus (NDV) in embryonating chicken eggs (ECE) was used as a diagnostic method. Fifteen field isolates obtained from presumptively infectious-bronchitis-affected chickens were analyzed by the IBV-NDV interference test. Eight isolates were capable of interfering with the growth of the La Sota strain of NDV, as measured by hemagglutination (HA) activity when IBV was inoculated 10 hr before NDV into ECE. The interference was considered specific for IBV, because it could be eliminated by adding homologous anti-IBV serum. The sensibility of this method could be demonstrated, because in some cases low-passage levels of IBV isolates showing HA interference ability were not capable of producing lesions in ECE. Furthermore, serologically negative IBV samples did not interfere with NDV growth. From these results, the IBV-NDV interference test appears to be a potential diagnostic alternative for identifying IBV field isolates.
Animals↗
Comparison of Sybr Green I, ELISA and conventional agarose gel-based PCR in the detection of infectious bursal disease virus.
The current available molecular method to detect infectious bursal disease virus (IBDV) is by reverse transcriptase-polymerase chain reaction (RT-PCR). However, the conventional PCR is time consuming, prone to error and less sensitive. In this study, the performances of Sybr Green I real-time PCR, enzyme-linked immunosorbent assay (ELISA) and conventional agarose detection methods in detecting specific IBDV PCR products were compared. We found the real-time PCR was at least 10 times more sensitive than ELISA detection method with a detection limit of 0.25pg. The latter was also at least 10 times more sensitive than agarose gel electrophoresis detection method. The developed assay detects both very virulent and vaccine strains of IBDV but not other RNA viruses such as Newcastle disease virus and infectious bronchitis virus. Hence, Sybr Green I-based real-time PCR is a highly sensitive assay for the detection of IBDV.
Animals↗
Specific and nonspecific immune responses to Marek's disease virus.
Marek's disease (MD) virus (MDV) has provided an important model to study immune responses against a lymphoma-inducing herpesvirus in its natural host. Infection in chickens starts with a lytic infection in B cells, followed by a latent infection in T cells and, in susceptible birds, T cell lymphomas develop. Non-specific and specific immune responses are important for the control of virus infection and subsequent tumor development. Interferon-gamma and nitric oxide are important for the control of virus replication during the lytic phase of infection and are also important to prevent reactivation of MDV replication in latently infected and transformed cells. Cytotoxic T cells (CTLs) are the most important of the specific immune responses in MDV. In addition to antigen-specific CTL against MDV proteins pp38, glycoprotein B (gB), Meq, and ICP4, ICP27-specific CTL can also be detected as early as 6 to 7 days post infection. The epitope for gB recognized by CTLs from P2a (MHC: B(19)B(19)) chickens has been localized to the Eco47III-BamHI (nucleotides 1515-1800) fragment. A proposed model for the interactions of cytokines and immune responses as part of the pathogenesis of MD is discussed.
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