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PubMed1987

Reducing agent-sensitive dimerization of the hemagglutinin-neuraminidase glycoprotein of Newcastle disease virus correlates with the presence of cysteine at residue 123.

Viruses within the Newcastle disease virus (NDV) serotype induce a wide array of disease manifestations ranging from an almost apathogenic pattern to the high mortality caused by avirulent or virulent isolates, respectively. A disulfide-linked dimer form of the NDV hemagglutinin-neuraminidase (HN) glycoprotein can be demonstrated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis under nonreducing conditions for only some of these isolates. For others, indeed the majority of those we have studied, no such reducing agent-sensitive dimeric form of HN is demonstrable. Apparently, there is no causal relationship between disulfide-linked dimeric HN and virulence. Using the deduced amino acid sequence of the dimeric HN of isolate AV as a basis for selection of oligonucleotide primers, we sequenced three additional reducing agent-sensitive dimeric HN glycoproteins and eight for which a disulfide-linked dimer has not been identified, using primer extension and dideoxy sequencing. The deduced amino acid sequences reveal a strict correlation between the presence of cysteine at residue 123 and reducing agent-sensitive dimerization of HN.

Amino Acid Sequence↗
PubMed1998

An attenuation mechanism of Newcastle disease vaccine strain TCND.

To provide information on the mechanism of attenuation of a Newcastle disease vaccine strain, TCND, we compared it with the parental virulent strain California 11,914 (CAL) biologically and genetically. It was found that TCND bore the fusion protein of virulent type, consisting of a pair of dibasic amino acid residues at the cleavage site and was a temperature sensitive (ts) mutant restricted to grow at 41.5 degrees C. Revertants were obtained by prolonged incubation of chicken embryos inoculated with TCND at the nonpermissive temperature. In cultured cells, viral gene transcription and protein synthesis of TCND occurred similarly to those of CAL and the revertants at 41.5 degrees C. Hemadsorption and immunofluorescence assays revealed that cell surface expression of functional hemagglutinin-neuraminidase (HN) of TCND at 41.5 degrees C was lower than that at 35 degrees C. The revertants exhibited lower activity in fusion assay than CAL and recovered virulence to chicken only in part. The results indicate that the ts mutation of TCND in association with the defect of HN glycoprotein transport is a mechanism of the attenuation, and in addition, some other factors such as fusion activity should be involved in the loss of virulence of CAL to chickens.

Amino Acid Sequence↗
PubMed1978

[Cytopathic effect of the Newcastle disease virus on the BHK-21 cell line].

The cytopathic effect (CPE) of the Newcastle disease virus (NDV) in the BNK-21 permenant cell line is studied in a series of experiments. The CPE is assessed as a percentage of hemadsorption and polykaryocytosis, and the dynamics of the viral replication is followed up with the aid of the immunofluorescent method. The effect of the cyclohexamide protein inhibitor of the replication of various NDV strains, on the CPE, respectively, is likewise studied. Five vellogenic, one mesogenic and one lentogenic strains are used in the experiments. It is found that through the immunofluorescent method the viral replication is delayed some three hrs in the case of the La Sota lentogenic strain in comparison with the other strains used. The direct relationship, already established, between the virulence of the NDV and the percentage of haemadsorption and polykaryocytosis is confirmed also in the BNC-21 heterologous cellular tissue. On the basis of this relationship, a rapid typing method of virulent from avirulent field NDV strains is suggested. The blocking effect of the cyclohexamide protein inhibitor on the CPE in NDV is demonstrated in the BNK-21 line, as a result of the blocking of the viral specific protein synthesis.

Animals↗
PubMed1975

Effects of bile and gastrointestinal secretions on the infectivity of Newcastle disease virus.

Bile aspirated from chicken gall bladders was found to contain substances neutralizing Newcastle disease virus (NDV). Nonspecific factors were present in the bile, probably the bile acids, which caused a reduction in the infectivity of the virus. Specific anti-NDV activity was found in the bile of birds that had been vaccinated with a lentogenic strain, Ulster, and challenged with a velogenic, viscerotropic strain, California 1083. Immunoglobulins were also found in these secretions and demonstrated to include the immunoglobulin A class as well as immunoglobulin G. Variability in the neutralizing capacity of bile was found with two different plaque clones of strain 1083, indicating antigenic heterogeneity in the viral population. No difference was found between bile from uninfected birds and the bile from NDV-immune birds in their activities against influenza strain Turkey Ontario 7732, whereas activity existed against a non-viscerotropic strain of NDV, Texas GB. These findings suggest that the specific activity of the secretions was most probably due to the presence of secretory antibody. The importance of the antiviral substances present in the alimentary tract was discussed with respect to the protection of the chicken against the viscerotropic pathotype of NDV.

Animals↗
PubMed1993

In vitro expansion and analysis of T lymphocyte microcultures obtained from the vaccination sites of cancer patients undergoing active specific immunization with autologous Newcastle-disease-virus-modified tumour cells.

In order to understand further the effects of Newcastle-disease-virus(NDV)-modified tumour vaccines we investigated the feasibility of isolating lymphocytes from the site of injection of patients undergoing postoperative active specific immunization (ASI) with autologous NDV-modified tumour cells. Delayed-type-hypersensitivity(DTH)-like reactions from five cancer patients were surgically removed, minced and the tissue particles were digested with collagenase and DNase. Lymphoid cells recovered were expanded in a highly efficient limiting-dilution analysis system optimized for T cell growth [Moretta et al. (1983) J Exp Med 157: 743] and lymphocyte microcultures (clonal probability > 0.8) could be grown for up to 1 year. Analysis of the microcultures for phenotype and function showed that the majority were positive for CD4 (92%) and TCR alpha beta (96%). Concanavalin-A-induced production of interleukin-2 (IL-2), IL-6, interferon gamma and tumour necrosis factor alpha was detected in more than 70% of the microcultures. Lectin-dependent cytotoxicity was only very rarely observed. The general characteristics of the microcultures obtained support the notion of a DTH-like reaction taking place at the site of tumour cell challenge. The possibility of in vitro expansion and cultivation of T lymphocytes from ASI vaccination sites should help to elucidate further the role of these cells in active specific immunization against autologous tumour cells.

Cells, Cultured↗
PubMedDate not supplied

Biological and molecular characterization of Newcastle disease virus isolates from surveillance of live bird markets in the northeastern United States.

Newcastle disease virus (NDV) is frequently recovered from surveillance samples collected by U.S. Department of Agriculture, Animal and Plant Health Inspection Service personnel in live bird markets. Six NDV isolates, five from chickens and one from a pheasant, were characterized for comparison with reference NDV isolates from poultry and other birds. All isolates tested were of low virulence for chickens. Four of the six isolates were similar to reference lentogens B1 and La Sota, but two isolates, one from a chicken and one from a pheasant, were different. The aberrant chicken isolate had a monoclonal antibody-binding profile like an unusual Canadian pigeon isolate. Sequence analysis of the matrix gene of this isolate demonstrated that it differed from all isolates included in the comparison and therefore may represent a third phylogenetic NDV group. The pheasant isolate had a monoclonal antibody-binding profile typical of other U.S. NDV lentogens but had a matrix gene sequence and hemagglutinin thermostability similar to strains Ulster and Queensland V4 (QV4), viruses originally isolated in Northern Ireland and Australia, respectively. The pheasant virus is the first lentogen isolated in the United States known to be closely related phylogenetically to Ulster and QV4. The unusual chicken and pheasant isolates were readily shed from the intestinal tract during chicken passage, whereas the other isolates were shed from the respiratory tract with little or no intestinal shedding. The frequency in live bird markets of viruses similar to those previously thought to be exotic to the United States in unknown.

Animals↗
PubMed1978

Cross-linking of Newcastle disease virus (NDV) proteins.

The proxomity and spatial relationships of the structural proteins of Newcastle disease virus (NDV) were studied by chemical cross-linking with a series of imidoesters. When the virions were reacted by the cross-linker with a distance 6.1A or longer between the functional groups and analyzed by polyacrylamide gel electrophoresis, remarkable changes were observed in the migration patterns of the viral proteins. The most striking one was the extensive decrease in the intensity of the M protein band, and although not so strikingly, glycoprotein and nucleocapsid protein bands were reduced significantly. Instead, several protein complexes appeared at and near the top of the gels. The protein complexes formed by a reversible cross-linker, dimethyl-3,3'-dithiobispropionimidate (DTBP), were analyzed by two dimensional electrophoresis; the complexes on the first-dimension cylindrical gels were cleaved by reduction with 2-mercaptoethanol and electrophoresed laterally on the second-dimension slab gels. The results indicated that homodimers of glycoprotein, nucleocapsid protein and M protein were generated under the condition of the most gentle cross-linking employed. At the same time, however, trimer and higher homopolymers of M protein were already detectable. Under the more extensive conditions, the bulk of M protein was cross-linked to form a large protein complex with very high molecular weight. Further, small but significant amounts of glycoprotein and nucleocapsid protein were always detected in this complex. These results suggest that M protein may be present in the virion in close enough proximity to interact with each other and may further have some interactions with glycoprotein and nucleocapsid protein. On the basis of these findings possible roles of M protein in virus assembly were discussed.

Dimethyl Adipimidate↗
PubMed1980

Maturation of the hemagglutinin-neuraminidase and fusion glycoproteins of two biologically distinct strains of Newcastle disease virus.

We have compared the glycoproteins of two biologically distinct virulent strains of Newcastle disease virus. Cells infected by either strain AV or HP produce infections virions and the cellular surfaces have hemadsorbing activity; however, only cells infected by strain AV undergo fusion from within. We fractionated chicken embryo cells and monitored the incorporation of radioactive proteins into virions to study the sites of synthesis, cellular locations, and kinetics of virion assembly for the hemagglutinin-neuraminidase (HN) and the fusion glycoproteins of each strain. We found that the HN glycoprotein of both strains was synthesized on rough endoplasmic reticulum (ER), accumulated in low-density membranes derived from smooth ER and the plasma membrane, and appeared in virions after a 30-min delay. The fusion glycoprotein of both strains was synthesized as a precursor in rough ER and subsequently processed to the active form. However, the sites of accumulation of the fusion glycoproteins were strain-dependent. The larger subunit F1 of the fusion glycoprotein of strain AV was detected in subcellular fractions enriched for plasma membranes, while that of strain HP accumulated in denser fractions which contained internal membranes. This result suggests that differential compartmentation of viral glycoproteins may influence the expression of biologic activities such as fusion on cellular surfaces. Despite their different sites of accumulation, the F1 glycoproteins or F-related polypeptides of similar size were assembled into virions of both strains. The kinetics of incorporation of this protein into virions appear to be too rapid for migration through internal membrane systems. Furthermore, tunicamycin did not block the incorporation of F-related polypeptides into virions. A hypothesis is presented to explain the unusual behavior of the F-related proteins.

Animals↗
PubMed1997

The effects of cyclosporin A and cyclophosphamide on the populations of B and T cells and virus in the Harderian gland of chickens vaccinated with the Hitchner B1 strain of Newcastle disease virus.

The cellular response to conjunctival vaccination with the Hitchner B1 strain of Newcastle disease virus was studied in the Harderian gland (HG) by immunohistochemistry. Bu-1+ cells and all subpopulations of T cells, (CD3+, CD4+, CD8+, TCR gamma delta, TCR alpha beta 1, and TCR alpha beta 2) were in the interstitial tissue between the ducts and the acini. Plasma cells with cytoplasmic IgM were more dispersed than the other cells and outlined the acini. Bu-1+ cells and all subpopulations of T cells increased at least three-fold after vaccination when compared to uninfected birds on the basis of the average cell counts in sections taken at 3, 5, 7, 10, 14, and 20 days after vaccination. The most marked increase was in the CD8+ cells which increased six-fold. Virus replicated for 10 days in cyclophosphamide (Cy) treated birds and for 7 days in cyclosporin A (CsA) treated birds compared with 5 days in untreated birds. Cy treatment prevented an antibody response to NDV and reduced Bu-1+ and IgM cells in the HG by 20-fold. Cy treatment resulted in a doubling of the number of T cells in the HG but these T cells may have been transiently disabled because it also caused a poor response of the lymphocytes in whole blood to the T cell mitogen concanavalin A (ConA). CsA reduced the T cell numbers in the HG and whole-blood responses to ConA by about 4-fold but T cell numbers rebounded to normal resting values after vaccination with NDV. The clearance time was prolonged either by T cells being less numerous than normal after CsA or being disabled after Cy. T cells, but not B cells, may therefore be essential for virus clearance. CD8+ cells expanded more than CD4+ cells after the vaccination of untreated and CsA-treated birds indicating that CD8+ cells may be key players in vaccinal immunity to NDV.

Animals↗
PubMed1994

The role of the individual cysteine residues in the formation of the mature, antigenic HN protein of Newcastle disease virus.

The amino acid sequence of the hemagglutinin-neuraminidase (HN) glycoprotein of Newcastle disease virus (NDV) has 14 cysteine residues, two of which are variably present in the sequences of the HN proteins of different strains of NDV while the rest are absolutely conserved. The role of each residue in the formation of the mature, oligomeric structure of the HN protein was assessed by characterizing proteins with mutations in each of the cysteine residues by Western analysis, immunoprecipitation with conformationally sensitive antibodies, immunofluorescence, and sedimentation on sucrose gradients. Proteins with mutations in the first cysteine (amino acid 6) or the second cysteine (amino acid 123), the nonconserved cysteine residues, formed antigenically mature oligomers which were transported to the cell surface like wild type. Protein with a mutation at cysteine 2 did not, however, form covalently linked oligomers demonstrating that it is this residue that is responsible for intermolecular disulfide bonds in the mature oligomer. Proteins with mutations in cysteine 3 (amino acid 172) or cysteine 5 (amino acid 196) formed proteins with all antigenic sites except one, site 23. These mutant proteins formed disulfide-linked dimers and were efficiently transported to the cell surface. They did not, however, sediment on gradients like the wild-type protein. They were also defective in the biological activities associated with the wild-type protein. Proteins with mutations in cysteines 4 (amino acid 186), 6 (amino acid 238), 7 (amino acid 247), 8 (amino acid 251), 13 (amino acid 531), or 14 (amino acid 542) contained no mature antigenic sites but formed noncovalently linked oligomers. Proteins with mutations in cysteines 9 (amino acid 344), 10 (amino acid 455), 11 (amino acid 461), or 12 (amino acid 465) formed proteins with antigenic site 4 but no other mature antigenic sites. These mutant proteins also formed noncovalently linked oligomers. These results suggest that mutations in different cysteine residues block the maturation of the HN protein at different stages.

Animals↗