scholarly journals Phosphoprotein Contributes to the Thermostability of Newcastle Disease Virus

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Yang Zhao ◽  
Huairan Liu ◽  
Feng Cong ◽  
Wei Wu ◽  
Ran Zhao ◽  
...  
Keyword(s):  
Newcastle Disease Virus ◽  
Disease Virus ◽  
Newcastle Disease ◽  
Reverse Genetics ◽  
Major Threat ◽  
P Protein ◽  
Growth Properties ◽  
Similar Growth ◽  
Thermostable Vaccine ◽  
Chimeric Viruses

Newcastle disease (ND), caused by Newcastle disease virus (NDV), is highly contagious and represents a major threat to the poultry industry. The thermostable vaccines are not insensitive to heat and ease of storage and transportation, but the mechanism of NDV thermostability remains unknown. The phosphoprotein (P), fusion protein (F), hemagglutinin-neuraminidase protein (HN), and large polymerase protein (L) are associated with NDV virulence. The association between F, HN, or L and viral thermostability has been, respectively, studied in different reports. However, the effects of P on NDV thermostability have not been demonstrated. Here, we utilized an existing reverse genetics system in our laboratory, to generate chimeric viruses by exchanging the P protein between the thermostable NDV4-C strain and the thermolabile LaSota strain. Chimeric viruses were found to possess similar growth properties, passage stability, and virulence, as compared to those of these parental strains. Interestingly, the thermostability of the chimera with P derived from the thermolabile LaSota strain was reduced compared to that of the parental virus, and P of the thermostable NDV4-C strain enhanced chimeric virus thermostability. Our data demonstrate that P is an important factor for the thermostability of NDV and provides information regarding the molecular mechanism of NDV thermostability; moreover, these results suggest a theoretical basis for using the NDV4-C strain as a thermostable vaccine.

scholarly journals The Hemagglutinin-Neuraminidase Protein of Newcastle Disease Virus Determines Tropism and Virulence

2004 ◽  
Vol 78 (8) ◽  
pp. 4176-4184 ◽  
Author(s):  
Zhuhui Huang ◽  
Aruna Panda ◽  
Subbiah Elankumaran ◽  
Dhanasekaran Govindarajan ◽  
Daniel D. Rockemann ◽  
...  
Keyword(s):  
Newcastle Disease Virus ◽  
Disease Virus ◽  
Newcastle Disease ◽  
Reverse Genetics ◽  
Index Test ◽  
Death Time ◽  
Virulent Virus ◽  
Hn Gene ◽  
Chimeric Viruses

ABSTRACT The hemagglutinin-neuraminidase (HN) protein of Newcastle disease virus (NDV) plays a crucial role in the process of infection. However, the exact contribution of the HN gene to NDV pathogenesis is not known. In this study, the role of the HN gene in NDV virulence was examined. By use of reverse genetics procedures, the HN genes of a virulent recombinant NDV strain, rBeaudette C (rBC), and an avirulent recombinant NDV strain, rLaSota, were exchanged. The hemadsorption and neuraminidase activities of the chimeric viruses showed significant differences from those of their parental strains, but heterotypic F and HN pairs were equally effective in fusion promotion. The tissue tropism of the viruses was shown to be dependent on the origin of the HN protein. The chimeric virus with the HN protein derived from the virulent virus exhibited a tissue predilection similar to that of the virulent virus, and vice versa. The chimeric viruses with reciprocal HN proteins either gained or lost virulence, as determined by a standard intracerebral pathogenicity index test of chickens and by the mean death time in chicken embryos (a measure devised to classify these viruses), indicating that virulence is a function of the amino acid differences in the HN protein. These results are consistent with the hypothesis that the virulence of NDV is multigenic and that the cleavability of F protein alone does not determine the virulence of a strain.

scholarly journals The Large Polymerase Protein Is Associated with the Virulence of Newcastle Disease Virus

2008 ◽  
Vol 82 (16) ◽  
pp. 7828-7836 ◽  
Author(s):  
Subrat N. Rout ◽  
Siba K. Samal
Keyword(s):  
Newcastle Disease Virus ◽  
Disease Virus ◽  
Newcastle Disease ◽  
Reverse Genetics ◽  
Severe Disease ◽  
Chimeric Virus ◽  
Minor Role ◽  
A Minor ◽  
Viral Determinants ◽  
Chimeric Viruses

ABSTRACT Naturally occurring Newcastle disease virus (NDV) strains vary greatly in virulence, ranging from no apparent infection to severe disease causing 100% mortality in chickens. The viral determinants of NDV virulence are not completely understood. Cleavage of the fusion protein is required for the initiation of infection, and it acts as a determinant of virulence. The attachment protein HN was found to play a minor role in virulence. In this study, we have evaluated the role of the internal proteins (N, P, and L) in NDV virulence by using a chimeric reverse-genetics approach. The N, P, and L genes were exchanged individually between an avirulent NDV strain, LaSota, and an intermediate virulent NDV strain, Beaudette C (BC), and the N and P genes were also exchanged together. The recovered chimeric viruses were evaluated for their pathogenicity in the natural host, chickens. Our results showed that the pathogenicities of N and P chimeric viruses were similar to those of their respective parental viruses, indicating that the N and P genes probably play minor roles in virulence. However, replacement of the L gene of BC with that of LaSota significantly increased the pathogenicity of the L-chimeric virus, suggesting that the L gene probably contributes to the virulence of NDV. The L-chimeric BC virus was found to replicate at a 100-fold-higher level than its parental virus in chicken brain, suggesting that the increase in pathogenicity may be due to the increased replication level of the chimeric virus. Our findings offer new insights into the pathogenesis of NDV infection.

Use of Reverse Genetics to Enhance the Oncolytic Properties of Newcastle Disease Virus

2007 ◽  
Vol 67 (17) ◽  
pp. 8285-8292 ◽  
Author(s):  
Adam Vigil ◽  
Man-Seong Park ◽  
Osvaldo Martinez ◽  
Mark A. Chua ◽  
Sa Xiao ◽  
...  
Keyword(s):  
Newcastle Disease Virus ◽  
Disease Virus ◽  
Newcastle Disease ◽  
Reverse Genetics

scholarly journals Reverse Genetics Assembly of Newcastle Disease Virus Genome Template Using Asis-Sal-Pac BioBrick Strategy

2020 ◽  
Vol 22 (1) ◽  
Author(s):  
Amin Tavassoli ◽  
Safoura Soleymani ◽  
Alireza Haghparast ◽  
Gholamreza Hashemi Tabar ◽  
Mohammad Reza Bassami ◽  
...  
Keyword(s):  
Newcastle Disease Virus ◽  
Disease Virus ◽  
Newcastle Disease ◽  
Reverse Genetics ◽  
Virus Genome

scholarly journals An improved method for the rescue of recombinant Newcastle disease virus

BioTechniques ◽  
2020 ◽  
Vol 68 (2) ◽  
pp. 96-100
Author(s):  
Pheik-Sheen Cheow ◽  
Tiong Kit Tan ◽  
Adelene Ai-Lian Song ◽  
Khatijah Yusoff ◽  
Suet Lin Chia
Keyword(s):  
Newcastle Disease Virus ◽  
Disease Virus ◽  
Newcastle Disease ◽  
Reverse Genetics ◽  
Vaccine Development ◽  
Transfection Efficiency ◽  
Transfection Method ◽  
Helper Plasmids ◽  
Immunogenic Properties ◽  
Recombinant Newcastle Disease Virus

Reverse genetics has been used to generate recombinant Newcastle disease virus with enhanced immunogenic properties for vaccine development. The system, which involves co-transfecting the viral antigenomic plasmid with three helper plasmids into a T7 RNA polymerase-expressing cell to produce viral progenies, poses a great challenge. We have modified the standard transfection method to improve the transfection efficiency of the plasmids, resulting in a higher titer of virus progeny production. Two transfection reagents (i.e., lipofectamine and polyethylenimine) were used to compare the transfection efficiency of the four plasmids. The virus progenies produced were quantitated with flow cytometry analysis of the infectious virus unit. The modified transfection method increased the titer of virus progenies compared with that of the standard transfection method.

Rescue of recombinant Newcastle disease virus: a promising vector with two decades of intensive vaccine research

2019 ◽  
Vol 14 (9) ◽  
pp. 617-628 ◽  
Author(s):  
Aidin Molouki ◽  
Abdou Nagy
Keyword(s):  
Newcastle Disease Virus ◽  
Disease Virus ◽  
Newcastle Disease ◽  
Reverse Genetics ◽  
Progeny Virus ◽  
Vaccine Research ◽  
Human Use ◽  
Helper Plasmids ◽  
Initiation Sequence ◽  
Recombinant Newcastle Disease Virus

Two decades have passed since the first reverse genetics system for the rescue of recombinant Newcastle disease virus was developed. Since then, the recombinant Newcastle disease virus vector has shown promising results as a safe and potent vector for development of many vaccines for both avian and human use. Herein, we review several technical topics that would be useful to further understanding of this technology. First, the effect of using helper plasmids encoding proteins belonging to strains other than the full-length cDNA and the possible incorporation of these expressed proteins into progeny virus will be discussed. Then, we will discuss the effect of removal of additional G residues from the T7 initiation sequence and finally, we will review different ways to improve rescue efficiency.

scholarly journals Newcastle disease virus fusion and haemagglutinin-neuraminidase proteins contribute to its macrophage host range

2013 ◽  
Vol 94 (6) ◽  
pp. 1189-1194 ◽  
Author(s):  
Ingrid Cornax ◽  
Diego G. Diel ◽  
Cary A. Rue ◽  
Carlos Estevez ◽  
Qingzhong Yu ◽  
...  
Keyword(s):  
Newcastle Disease Virus ◽  
Host Range ◽  
Cell Line ◽  
Disease Virus ◽  
Newcastle Disease ◽  
Fibroblast Cell ◽  
Fibroblast Cell Line ◽  
Multifunctional Proteins ◽  
Virus Fusion ◽  
Chimeric Viruses

The fusion (F) and haemagglutinin-neuraminidase (HN) proteins of Newcastle disease virus (NDV) are multifunctional proteins that play critical roles during infection. Here, we assessed the ability of NDV to replicate in macrophages and investigated the contribution of the F and HN proteins to NDV infection/replication in these cells. Results of our study revealed that, while presenting similar replication kinetics in a fibroblast cell line (DF1) or in primary non-adherent splenocytes, the NDV strain CA02 replicates better in macrophages (HD11 and primary adherent splenocytes) than the NDV strain Anhinga/93. Notably, exchange of the HN or both F and HN genes of NDV Anhinga/93 by the corresponding genes from NDV CA02 markedly improved the ability of the chimeric viruses to replicate in macrophages. These results indicate that the F and HN proteins are determinants of NDV macrophage host range. This represents the first description of productive NDV infection in macrophages.

scholarly journals Patterns of RNA Editing in Newcastle Disease Virus Infections

Viruses ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 1249
Author(s):  
Archana Jadhav ◽  
Lele Zhao ◽  
Alice Ledda ◽  
Weiwei Liu ◽  
Chan Ding ◽  
...  
Keyword(s):  
Newcastle Disease Virus ◽  
Rna Editing ◽  
Disease Virus ◽  
Newcastle Disease ◽  
Structural Proteins ◽  
Virus Infections ◽  
Mrna Editing ◽  
P Protein

The expression of accessory non-structural proteins V and W in Newcastle disease virus (NDV) infections depends on RNA editing. These proteins are derived from frameshifts of the sequence coding for the P protein via co-transcriptional insertion of one or two guanines in the mRNA. However, a larger number of guanines can be inserted with lower frequencies. We analysed data from deep RNA sequencing of samples from in vitro and in vivo NDV infections to uncover the patterns of mRNA editing in NDV. The distribution of insertions is well described by a simple Markov model of polymerase stuttering, providing strong quantitative confirmation of the molecular process hypothesised by Kolakofsky and collaborators three decades ago. Our results suggest that the probability that the NDV polymerase would stutter is about 0.45 initially, and 0.3 for further subsequent insertions. The latter probability is approximately independent of the number of previous insertions, the host cell, and viral strain. However, in LaSota infections, we also observe deviations from the predicted V/W ratio of about 3:1 according to this model, which could be attributed to deviations from this stuttering model or to further mechanisms downregulating the abundance of W protein.

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