Lysis of Myelocytes in Chickens Infected with Infectious Bursal Disease Virus

Fujita, Akihiro; Maeda, Ken

doi:10.1354/vp.36-2-146

Cited by 11 publications

(6 citation statements)

References 23 publications

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“…Lytic infection of IBDV in premature B lymphocyte was considered as the pathogenesis of IBDV-related disease 41 42 . However, the detailed molecular mechanism of cell lysis at the late stage of viral infection is still unclear.…”

Section: Discussionmentioning

confidence: 99%

The C-terminal amyloidogenic peptide contributes to self-assembly of Avibirnavirus viral protease

Zheng

Jia

et al. 2015

Sci Rep

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Unlike other viral protease, Avibirnavirus infectious bursal disease virus (IBDV)-encoded viral protease VP4 forms unusual intracellular tubule-like structures during viral infection. However, the formation mechanism and potential biological functions of intracellular VP4 tubules remain largely elusive. Here, we show that VP4 can assemble into tubules in diverse IBDV-infected cells. Dynamic analysis show that VP4 initiates the assembly at early stage of IBDV infection, and gradually assembles into larger size of fibrils within the cytoplasm and nucleus. Intracellular assembly of VP4 doesn’t involve the host cytoskeleton, other IBDV-encoded viral proteins or vital subcellular organelles. Interestingly, the last C-terminal hydrophobic and amyloidogenic stretch 238YHLAMA243 with two “aggregation-prone” alanine residues was found to be essential for its intracellular self-assembly. The assembled VP4 fibrils show significantly low solubility, subsequently, the deposition of highly assembled VP4 structures ultimately deformed the host cytoskeleton and nucleus, which was potentially associated with IBDV lytic infection. Importantly, the assembly of VP4 significantly reduced the cytotoxicity of protease activity in host cells which potentially prevent the premature cell death and facilitate viral replication. This study provides novel insights into the formation mechanism and biological functions of the Avibirnavirus protease-related fibrils.

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Section: Discussionmentioning

confidence: 99%

The C-terminal amyloidogenic peptide contributes to self-assembly of Avibirnavirus viral protease

Zheng

Jia

et al. 2015

Sci Rep

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“…Histological diagnosis is based on the detection of modifications occurring in the bursa. The ability to cause histological lesions in the non-bursal lymphoid organs, such as the thymus spleen or bone marrow [46] has been described as a possible characteristic of hypervirulent IBDV strains. The histological diagnostic method has the advantage of allowing for the diagnosis of both the acute and chronic or subclinical forms of the disease.…”

Section: Histological Diagnosismentioning

confidence: 99%

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2023

EIJ

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Chickens rising have long been a line of tradition and the large numbers of chicken populations are kept in the backyard production system in Ethiopia. Poultry disease is among the main constraints of poultry production in the country. The infectious bursal disease is widespread viral diseases that affect chicken kept in commercial and backyard production system. Infectious bursal disease virus is a primary affect bursa fabricia of young chicken and is host-specific. This virus is prone to mutation, extremely stable and unaffected by chemicals and disinfectant. The most common route of infection is oral, conjunctiva and respiratory. The infectious bursal disease is extremely contagious and its severity is depends on age, breed of the affected birds, the degree of passive immunity and the virulence of the strain of the virus, and secondary infections associated with the immunosuppressive effects of the disease. Control of the disease has been more difficult by the popularity of variant strains of the infectious bursal disease virus. Variant viruses induce damage within the bursa fabricia in chickens, even once high and uniform protein titers are presence. The infectious bursal disease has an enormous economic impact on production varying from direct to indirect losses. Direct losses of disease are due to mortality and the financial losses due to reduced production parameters as a result of subclinical infections. The indirect economic impact of the disease is immunological disorder, growth retardation and condemnation of carcasses. With proper use of vaccine and vaccination program together with other measures like sanitation, good nutrient, high level of management in poultry farms was suggested.

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“…Στα νε κροτομή θέντα πτηνά παρατηρούνται επίσης αφυδάτωση, διογκωμένοι νεφροί με υπόλευκο περιεχόμενο εναποθέ σεων ουρικών αλάτων, γραμμοειδείς αιμορραγίες στην επιφάνεια των μηρών, του στέρνου και της κνήμης, που συνενοΰμενες εμφανίζονται ως μεγάλες αιμορραγικές εστίες. Ακόμη, στις οξείες μορφές της IBD από τα πολΰ λοιμογόνα στελέχη μπορεί να παρατηρηθούν μακροσκο πικές αλλοιώσεις στο θΰμο αδένα, τη σπλήνα, τις τυφλικές αμυγδαλές, τους αδένες του Harder, τις πλάκες του Payer και το μυελό των οστών (Inoue et al 1999, Tsukamoto et al 1995.…”

Section: κλινικη εικονα της νοσουunclassified

“…Βασίζε ται στην ανεΰρεση αλλοιώσεων που συμβαίνουν στο θΰ λακο, αλλά και σε άλλα όργανα, όπως ο θΰμος αδένας, η σπλήνα και ο μυελός των οστών (Inoue et al 1999, Bougiouklis et al 2001. Η ιστολογική εξέταση έχει το πλεονέκτημα της επιβεβαίωσης της διάγνωσης και των δΰο μορφών (οξείας και υποκλινικής IBD).…”

Section: εργαστηριακή α) ιστολογική εξέτασηunclassified

Gumboro disease (IBD)

Georgopoulou

2017

J Hellenic Vet Med Soc

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Gumboro Disease (IBD) caused by Infectious Bursal Disease Virus is an immunosuppressive condition of chickens, which resulted in severe economical losses. Approximately 47 years after the first appearance of the disease, the changes in the form of presentation and pathogenicity of IBDV in the field has resulted in continual changes and adjustments of the vaccines used to control IBD. The original form of the disease, also known as classic or clinical IBD, was usually observed after the third week of life with high mortality, depending on factors, such as virulence of the strain of virus involved, age of the birds and maternal antibody status. The acute IBD is caused by the very virulent IBDV strains, characterized by high mortality rates in vaccinated chickens and the clinical signs and lesions are similar to those of the classic form. The subclinicalform of the disease is associated with the "variant" strains of IBDV and is characterized by low mortality and severe immunosuppression. Initially, the classic IBD was controlled by the use of mild vaccines produced in the early 1970s and from the late 1980s revealed absence of protection from wIBDV in vaccinated chickens. Another group of vaccinal strains, known as intermediate plus vaccine, has been used to control wIBDV strains. These vaccines multiply in birds, even in the presence of high maternal antibody titers. In the USA and other countries, the disease from the variant strains was controlled by intermediate strains as well as by inactivated vaccines that included variant strains, thus providing maternal antibodies against both the standard and variant strains. Until today, the IBD continues to pose an important threat to commercial poultry industry. The high resistence of IBDV to physical and chemical agents accounts for persistence of the virus in the outside environment, particularly on contaminated farms, despite disinfection. Nevertheless and not quite unexpected for the IBDV mutations in the genome, resulted in the emergence of antigenic variant strains in vaccinated flocks. The IBD requires heightened vigilance and the incidence and prevalence of the clinical and immunosuppressive forms must be evaluated more precisely.

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Lysis of Myelocytes in Chickens Infected with Infectious Bursal Disease Virus

Cited by 11 publications

References 23 publications

The C-terminal amyloidogenic peptide contributes to self-assembly of Avibirnavirus viral protease

The C-terminal amyloidogenic peptide contributes to self-assembly of Avibirnavirus viral protease

Untitled

Gumboro disease (IBD)

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