scholarly journals Genomic sequence of infectious bursal disease virus from Zambia suggests evidence for genome re-assortment in nature

Author(s):  
Christopher J. Kasanga ◽  
T. Yamaguchi ◽  
H.M. Munang’andu ◽  
P.N. Wambura ◽  
K. Ohya ◽  
...  

Infectious bursal disease virus (IBDV) is a bi-segmented RNA virus, which belongs to the genus Avibirnavirus of the family Birnaviridae. Two serotypes, 1 and 2, exist in IBDV. The serotype 1 IBDVs are the causative agents of infectious bursal disease (IBD) in chickens worldwide and lead to immunosuppression in young birds. Genome re-assortment has been speculated to occur and contribute to the emergence of new IBDV strains. However, evidence was lacking until recently when two re-assortant viruses were detected in China. In this study, we determined the complete nucleotide sequence of an IBDV, designated KZC-104, from a confirmed natural IBD outbreak in Lusaka, Zambia in 2004. The genome consisted of 3074 and 2651 nucleotides in the coding regions of segments A and B, respectively. Alignment of both nucleotide and deduced amino acid sequences, and phylogenetic analysis revealed that the genome segment A of KZC-104 was derived from a very virulent strain, whereas its segment B was derived from a classical attenuated strain. On BLAST search, the full-length segments A and B sequences showed 98% closest nucleotide homology to the very virulent strain D6948 and 99.8% closest nucleotide homology to the classical attenuated strain D78, respectively. This is a unique IBDV reassortant strain, which has emerged in nature involving segment B of a live attenuated vaccine. This observation provides direct evidence for the involvement of vaccine strains in the emergence of reassortant IBDV in the field. Taken together, these findings suggest an additional risk of using live IBDV vaccines, which may act as genetic donors for genome re-assortment. Further studies are required to investigate the epidemiology and biological characteristics of reassortant strains so that the appropriate and safe IBDV vaccines can be recommended.

2002 ◽  
Vol 147 (7) ◽  
pp. 1303-1322 ◽  
Author(s):  
M. F. Rudd ◽  
H. G. Heine ◽  
S. I. Sapats ◽  
L. Parede ◽  
J. Ignjatovic

2009 ◽  
Vol 386 (3) ◽  
pp. 891-901 ◽  
Author(s):  
Daniel Luque ◽  
Irene Saugar ◽  
María Teresa Rejas ◽  
José L. Carrascosa ◽  
José F. Rodríguez ◽  
...  

2016 ◽  
Vol 46 (1) ◽  
pp. 19-27 ◽  
Author(s):  
Sébastien M. Soubies ◽  
Céline Courtillon ◽  
François-Xavier Briand ◽  
Maryline Queguiner-Leroux ◽  
David Courtois ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Liliana L. Cubas-Gaona ◽  
Alexandre Flageul ◽  
Céline Courtillon ◽  
Francois-Xavier Briand ◽  
Maud Contrant ◽  
...  

The avibirnavirus infectious bursal disease virus (IBDV) is responsible for a highly contagious and sometimes lethal disease of chickens (Gallus gallus). IBDV genetic variation is well-described for both field and live-attenuated vaccine strains, however, the dynamics and selection pressures behind this genetic evolution remain poorly documented. Here, genetically homogeneous virus stocks were generated using reverse genetics for a very virulent strain, rvv, and a vaccine-related strain, rCu-1. These viruses were serially passaged at controlled multiplicities of infection in several biological systems, including primary chickens B cells, the main cell type targeted by IBDV in vivo. Passages were also performed in the absence or presence of a strong selective pressure using the antiviral nucleoside analog 7-deaza-2′-C-methyladenosine (7DMA). Next Generation Sequencing (NGS) of viral genomes after the last passage in each biological system revealed that (i) a higher viral diversity was generated in segment A than in segment B, regardless 7DMA treatment and viral strain, (ii) diversity in segment B was increased by 7DMA treatment in both viruses, (iii) passaging of IBDV in primary chicken B cells, regardless of 7DMA treatment, did not select cell-culture adapted variants of rvv, preserving its capsid protein (VP2) properties, (iv) mutations in coding and non-coding regions of rCu-1 segment A could potentially associate to higher viral fitness, and (v) a specific selection, upon 7DMA addition, of a Thr329Ala substitution occurred in the viral polymerase VP1. The latter change, together with Ala270Thr change in VP2, proved to be associated with viral attenuation in vivo. These results identify genome sequences that are important for IBDV evolution in response to selection pressures. Such information will help tailor better strategies for controlling IBDV infection in chickens.


2001 ◽  
Vol 75 (22) ◽  
pp. 10815-10828 ◽  
Author(s):  
José R. Castón ◽  
Jorge L. Martı́nez-Torrecuadrada ◽  
Antonio Maraver ◽  
Eleuterio Lombardo ◽  
José F. Rodrı́guez ◽  
...  

ABSTRACT Infectious bursal disease virus (IBDV), a member of the Birnaviridae family, is a double-stranded RNA virus. The IBDV capsid is formed by two major structural proteins, VP2 and VP3, which assemble to form a T=13 markedly nonspherical capsid. During viral infection, VP2 is initially synthesized as a precursor, called VPX, whose C end is proteolytically processed to the mature form during capsid assembly. We have computed three-dimensional maps of IBDV capsid and virus-like particles built up by VP2 alone by using electron cryomicroscopy and image-processing techniques. The IBDV single-shelled capsid is characterized by the presence of 260 protruding trimers on the outer surface. Five classes of trimers can be distinguished according to their different local environments. When VP2 is expressed alone in insect cells, dodecahedral particles form spontaneously; these may be assembled into larger, fragile icosahedral capsids built up by 12 dodecahedral capsids. Each dodecahedral capsid is an empty T=1 shell composed of 20 trimeric clusters of VP2. Structural comparison between IBDV capsids and capsids consisting of VP2 alone allowed the determination of the major capsid protein locations and the interactions between them. Whereas VP2 forms the outer protruding trimers, VP3 is found as trimers on the inner surface and may be responsible for stabilizing functions. Since elimination of the C-terminal region of VPX is correlated with the assembly of T=1 capsids, this domain might be involved (either alone or in cooperation with VP3) in the induction of different conformations of VP2 during capsid morphogenesis.


2017 ◽  
Vol 5 (34) ◽  
Author(s):  
Hyun-Jeong Lee ◽  
Il Jang ◽  
Sun-Hwa Shin ◽  
Hee-Soo Lee ◽  
Kang-Seuk Choi

ABSTRACT Here, we report the complete coding genome sequence of a novel reassortant and very virulent infectious bursal disease virus (IBDV), designated JBN2011. Characterization of the JBN2011 genome suggests that it is a rare recombinant virus having a very virulent IBDV segment A and a Bursine-2-like attenuated IBDV segment B.


2007 ◽  
Vol 123 (1) ◽  
pp. 50-56 ◽  
Author(s):  
Chi Wai Yip ◽  
Yin Shan Yeung ◽  
Ching Man Ma ◽  
Pui Yi Lam ◽  
Chung Chau Hon ◽  
...  

1996 ◽  
Vol 42 (1) ◽  
pp. 93-97 ◽  
Author(s):  
B. Qian ◽  
F. S. B. Kibenge

Previous analyses of the two serotypes of infectious bursal disease virus (IBDV) have demonstrated the correlation between antigenicity and similarities of nucleotide and amino acid sequences of the VP2 coding region in genome segment A. Restriction fragment profiles of genomic segment A cDNA of five IBDV isolates (QC-2 and QT-1 of serotype 1, SK9, and Nos. 39 and 52 of serotype 2) were determined in order to establish the genetic relationship of these viruses to other avibirnaviruses. The restriction fragment profiles using three of seven restriction enzymes (Sad which cuts in the VP2 region, DraIII which cuts in the VP3 region, and EcoRI which cuts in the VP4 region) were used to place QC-2, QT-1, SK9, No. 39, and No. 52 within the phylogenetic tree among seven other avibirnaviruses of known sequence. The two IBDV serotypes corresponded to two genotypes on the basis of the presence or absence of the SacI restriction site. The serotype 1 cluster of strains was further differentiated into five minor clusters on the basis of the PstI, EcoRI, BamHI, HindIII, DraIII, and Bsu36I restriction sites, which emphasized the geographical origins of the strains. It is concluded that restriction analysis of cDNA of the whole viral genomic segment A allows differentiation of IBDV isolates on the basis of their antigenicity and geographical origin.Key words: phylogeny, avibirnavirus, geographical origin.


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