Infectious Bursal Disease Virus non-structural protein VP5 is not a transmembrane protein

Carballeda, Juan Manuel; Maroniche, Guillermo Andrés; Lucero, María Soledad; Richetta, Matías; Gómez, Emma Laura Alfaro; Zoth, Silvina Andrea Chimeno; Berinstein, Analía

doi:10.1016/j.virol.2015.05.003

Cited by 7 publications

(5 citation statements)

References 24 publications

(26 reference statements)

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“…However, it migrates as a 17-kDa product on SDS-PAGE, thus suggesting that it might be post-translationally modified [15]. Despite the lack of a transmembrane domain, VP5 accumulates at the cytosolic leaflet of different membranous cell compartments, preferentially at the plasma membrane (PM) [17, 18]. This tropism is mediated by the interaction of the VP5 C-terminal polycationic protein region, known as the phosphoinositide (PIP)-binding domain, with integral membrane PIPs [17].…”

Section: Introductionmentioning

confidence: 99%

Non-Lytic Egression of Infectious Bursal Disease Virus (IBDV) Particles from Infected Cells

et al. 2017

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Infectious bursal disease virus (IBDV), a member of the Birnaviridae family, is responsible for a devastating immunosuppressive disease affecting juvenile domestic chickens. IBDV particles are naked icosahedrons enclosing a bipartite double-stranded RNA genome harboring three open reading frames (ORF). One of these ORFs codes for VP5, a non-structural polypeptide dispensable for virus replication in tissue culture but essential for IBDV pathogenesis. Using two previously described recombinant viruses, whose genomes differ in a single nucleotide, expressing or not the VP5 polypeptide, we have analyzed the role of this polypeptide during the IBDV replication process. Here, we show that VP5 is not involved in house-keeping steps of the virus replication cycle; i.e. genome transcription/replication, protein translation and virus assembly. Although infection with the VP5 expressing and non-expressing viruses rendered similar intracellular infective progeny yields, striking differences were detected on the ability of their progenies to exiting infected cells. Experimental data shows that the bulk of the VP5-expressing virus progeny efficiently egresses infected cells during the early phase of the infection, when viral metabolism is peaking and virus-induced cell death rates are as yet minimal, as determined by qPCR, radioactive protein labeling and quantitative real-time cell death analyses. In contrast, the release of the VP5-deficient virus progeny is significantly abridged and associated to cell death. Taken together, data presented in this report show that IBDV uses a previously undescribed VP5-dependent non-lytic egress mechanism significantly enhancing the virus dissemination speed. Ultrastructural analyses revealed that newly assembled IBDV virions associate to a vesicular network apparently facilitating their trafficking from virus assembly factories to the extracellular milieu, and that this association requires the expression of the VP5 polypeptide.

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Section: Introductionmentioning

confidence: 99%

Non-Lytic Egression of Infectious Bursal Disease Virus (IBDV) Particles from Infected Cells

et al. 2017

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“…Therefore, additional research is required to fully elucidate the roles of VP2 and VP5 in the virulence of IPNV infection. The VP5 sequence does contain the Bcl-2 homology (BH) domains BH1, BH2, BH3, and BH4 typical of class I and II Bcl-2 family proteins [ 21 , 22 ]. Accurate understandings on the role of these sequences in the cellular infection mechanism remain lacking, as is also the case for the functional effects of structural motif variations in VP5.…”

Section: Introductionmentioning

confidence: 99%

Molecular characterization of infectious pancreatic necrosis virus strains isolated from the three types of salmonids farmed in Chile

Manríquez

Vera

Villalba

et al. 2017

Virol J

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BackgroundThe infectious pancreatic necrosis virus (IPNV) causes significant economic losses in Chilean salmon farming. For effective sanitary management, the IPNV strains present in Chile need to be fully studied, characterized, and constantly updated at the molecular level.MethodsIn this study, 36 Chilean IPNV isolates collected over 6 years (2006–2011) from Salmo salar, Oncorhynchus mykiss, and Oncorhynchus kisutch were genotypically characterized. Salmonid samples were obtained from freshwater, estuary, and seawater sources from central, southern, and the extreme-south of Chile (35° to 53°S).ResultsSequence analysis of the VP2 gene classified 10 IPNV isolates as genogroup 1 and 26 as genogroup 5. Analyses indicated a preferential, but not obligate, relationship between genogroup 5 isolates and S. salar infection. Fifteen genogroup 5 and nine genogroup 1 isolates presented VP2 gene residues associated with high virulence (i.e. Thr, Ala, and Thr at positions 217, 221, and 247, respectively). Four genogroup 5 isolates presented an oddly long VP5 deduced amino acid sequence (29.6 kDa). Analysis of the VP2 amino acid motifs associated with clinical and subclinical infections identified the clinical fingerprint in only genogroup 5 isolates; in contrast, the genogroup 1 isolates presented sequences predominantly associated with the subclinical fingerprint. Predictive analysis of VP5 showed an absence of transmembrane domains and plasma membrane tropism signals. WebLogo analysis of the VP5 BH domains revealed high identities with the marine birnavirus Y-6 and Japanese IPNV strain E1-S. Sequence analysis for putative 25 kDa proteins, coded by the ORF between VP2 and VP4, exhibited three putative nuclear localization sequences and signals of mitochondrial tropism in two isolates.ConclusionsThis study provides important advances in updating the characterizations of IPNV strains present in Chile. The results from this study will help in identifying epidemiological links and generating specific biotechnological tools for controlling IPNV outbreaks in Chilean salmon farming.

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“…The literature reported that VP5 is a phosphoinositidebinding protein and demonstrated that VP5 protein is essential for the spread of the virus among cells (Méndez et al, 2015). Although topological prediction analysis revealed that VP5 protein may be a type II transmembrane protein, including potential transmembrane and intracellular N-terminal and C-terminal structures, the latest findings clearly indicate that VP5 is not a transmembrane protein (Carballeda et al, 2015). Therefore, the role of VP5 protein in the release of virions remains to be further studied.…”

Section: Vp5mentioning

confidence: 99%

Molecular Biology, Immunosuppression and Pathogenesis of Infectious Bursal Disease Virus

Hussain¹,

Ashraf²,

Shamim³

et al. 2021

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Infectious bursal disease (IBD), caused by infectious bursal disease virus (IBDV), is one of the most devastating and immunosuppressive diseases of the poultry and has been a constraint on the sustainable food security around the globe including Pakistan. Poultry industry is the second biggest industry in Pakistan while IBD is an important disease seriously threatening poultry farming. Despite the use of mass and intense vaccination regimens, the disease continues to sustain in many countries around the globe including Pakistan. However, to some extent, the epidemic strains and epidemic patterns predominant strains of IBDV in Pakistan is unclear. This highlights the need to characterize field strains of IBDV to ascertain the evidence of vaccine failure and to establish foundations for the development of vaccine matching with the epidemic strains.

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Infectious Bursal Disease Virus non-structural protein VP5 is not a transmembrane protein

Cited by 7 publications

References 24 publications

Non-Lytic Egression of Infectious Bursal Disease Virus (IBDV) Particles from Infected Cells

Non-Lytic Egression of Infectious Bursal Disease Virus (IBDV) Particles from Infected Cells

Molecular characterization of infectious pancreatic necrosis virus strains isolated from the three types of salmonids farmed in Chile

Molecular Biology, Immunosuppression and Pathogenesis of Infectious Bursal Disease Virus

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