scholarly journals Molecular epidemiology of infectious bursal disease virus in Zambia

2013 ◽  
Vol 84 (1) ◽  
Author(s):  
Christopher J. Kasanga ◽  
Tsuyoshi Yamaguchi ◽  
Hetron M. Munang’andu ◽  
Kenji Ohya ◽  
Hideto Fukushi
Keyword(s):  
Phylogenetic Analysis ◽  
Amino Acid ◽  
Infectious Bursal Disease Virus ◽  
Hypervariable Region ◽  
Distinct Group ◽  
The Other ◽  
Infectious Bursal Disease ◽  
Western Africa ◽  
Infectious Bursal Disease Viruses ◽  
Bursal Disease

Nucleotide sequences of the VP2 hypervariable region (VP2-HVR) of 10 infectious bursal disease viruses detected in indigenous and exotic chickens in Zambia from 2004 to 2005 were determined. Phylogenetic analysis showed that the viruses diverged into two genotypes and belonged to the African very virulent types (VV1 and VV2). In the phylogenetic tree, strains in one genotype clustered in a distinct group and were closely related to some strains isolated in western Africa (VV1), with nucleotide similarities of 95.7%– 96.5%. Strains in the other genotype were clustered within the eastern African VV type (VV2), with nucleotide similarities of 97.3%– 98.5%. Both genotypes were distributed in the southern parts of Zambia and had a unique conserved amino acid substitution at 300 (E→A) in addition to the putative virulence marker at positions 222(A), 242(I), 256(I), 294(I) and 299(S). These findings represent the first documentation of the existence of the African VV-IBDV variants in both indigenous and exotic chickens in Zambia.

Molecular characterisation of infectious bursal disease viruses isolated in recent acute outbreaks in Solvenia

2008 ◽  
Vol 56 (2) ◽  
pp. 255-264 ◽  
Author(s):  
Olga Zorman Rojs ◽  
Uroš Krapež ◽  
Brigita Slavec ◽  
Sara Mankoč ◽  
Rahela Jurišič-Cizerl ◽  
...  
Keyword(s):  
Amino Acid ◽  
Phylogenetic Analyses ◽  
Hypervariable Region ◽  
Infectious Bursal Disease ◽  
Amino Acid Substitutions ◽  
Molecular Characterisation ◽  
Broiler Breeder ◽  
Infectious Bursal Disease Viruses ◽  
Bursal Disease ◽  
Serotype 1

In 2004 and then in 2006 several outbreaks of infectious bursal disease (IBD) were reported in broiler and broiler breeder flocks in Slovenia. In this report ten recently emerged IBD viruses (IBDV) were characterised by sequence analysis of the VP2 hypervariable region and compared to previous Slovene IBDV strains from 1995/1996 and to some representative serotype 1 IBDV strains of different pathotypes. On the basis of nucleotide and amino acid identities, phylogenetic analyses and the presence of very virulent IBDV (vvIBDV) conserved amino acid substitutions, all Slovene isolates from recent outbreaks were identified as vvIBDV. Although some unique nucleotide exchanges and amino acid substitutions have been observed, the results of this study indicated that recent vvIBDV isolates are closely related with those from outbreaks in the 1990s. However, acute IBD has not been reported in commercial flocks in Slovenia for some years. This could lead to the conclusion that poor biosecurity and relaxed vaccination could be responsible for the re-emergence of vvIBDV.

scholarly journals Alteration of amino acids in VP2 of very virulent infectious bursal disease virus results in tissue culture adaptation and attenuation in chickens

2002 ◽  
Vol 83 (1) ◽  
pp. 121-129 ◽  
Author(s):  
A. A. W. M. van Loon ◽  
N. de Haas ◽  
I. Zeyda ◽  
E. Mundt
Keyword(s):  
Amino Acids ◽  
Tissue Culture ◽  
Amino Acid ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Site Directed Mutagenesis ◽  
Infectious Bursal Disease ◽  
Single Amino Acid ◽  
Culture Adaptation ◽  
Bursal Disease

Reverse genetics technology offers the possibility to study the influence of particular amino acids of infectious bursal disease virus (IBDV) on adaptation to tissue culture. Genomic segments A and B of the very virulent (vv) IBDV field strain UK661 were completely cloned and sequenced, and the strain was rescued from full-length cDNA copies of both segments (UK661rev). Using site-directed mutagenesis, alteration of a single amino acid in the segment A-encoded VP2 (A284T) resulted in a limited capacity of UK661 to replicate in tissue culture. Additional alteration of a second amino acid (Q253H) increased replication efficiency in tissue culture. The second mutant (UK661-Q253H-A284T) was used to infect chickens and results were compared with UK661 and UK661rev. Whereas UK661 and UK661rev induced 100% morbidity and 50–80% mortality, UK661-Q253H-A284T proved to be strikingly attenuated, producing neither morbidity nor mortality. Moreover, UK661-Q253H-A284T-infected animals were protected from challenge infection. Thus, alteration of two specific amino acids in the VP2 region of IBDV resulted in tissue culture adaptation and attenuation in chickens of vvIBDV. The data demonstrate that VP2 plays a decisive role in pathogenicity of IBDV.

scholarly journals Sequence analysis of VP2 hypervariable region of the field isolates of infectious bursal disease viruses from southern region of India

2018 ◽  
Vol 62 (01) ◽  
pp. 86-97 ◽  
Author(s):  
P. RAJA ◽  
T. M. A. SENTHILKUMAR ◽  
C. V. PRIYADARSHINI ◽  
M. PARTHIBAN ◽  
A. THANGAVELU ◽  
...  
Keyword(s):  
Sequence Analysis ◽  
Hypervariable Region ◽  
Southern Region ◽  
Infectious Bursal Disease ◽  
Field Isolates ◽  
Infectious Bursal Disease Viruses ◽  
Bursal Disease

scholarly journals Molecular characterisation of infectious bursal disease virus in Namibia, 2017

2019 ◽  
Vol 86 (1) ◽  
Author(s):  
Umberto Molini ◽  
Gottlieb Aikukutu ◽  
Juliet Kabajani ◽  
Siegfried Khaiseb ◽  
Giovanni Cattoli ◽  
...  
Keyword(s):  
Phylogenetic Analysis ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Infectious Bursal Disease ◽  
Partial Sequence ◽  
Molecular Characterisation ◽  
Rt Pcr ◽  
Bursal Disease ◽  
Control And Management

Between July and September 2017, samples collected from six unvaccinated chickens in Namibia were shown to be positive for infectious bursal disease virus (IBDV) by RT-PCR. Partial sequence and phylogenetic analysis of the VP1 and VP2 genes from six viruses revealed that they all belong to the very virulent pathotype (Genogroup 3) and are genetically very similar to IBDVs identified in neighbouring Zambia. This is the first molecular characterisation of IBDV in Namibia and has implications on the control and management of the disease in the country.

scholarly journals Phylogenetic Analysis Reveals a Correlation between the Expansion of Very Virulent Infectious Bursal Disease Virus and Reassortment of Its Genome Segment B

2006 ◽  
Vol 80 (17) ◽  
pp. 8503-8509 ◽  
Author(s):  
Chung-Chau Hon ◽  
Tsan-Yuk Lam ◽  
Alexei Drummond ◽  
Andrew Rambaut ◽  
Yiu-Fai Lee ◽  
...  
Keyword(s):  
Phylogenetic Analysis ◽  
Population Dynamics ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Genome Segment ◽  
Infectious Bursal Disease ◽  
Reassortment Event ◽  
The Past ◽  
Bursal Disease ◽  
Past Population

ABSTRACT Infectious bursal disease virus (IBDV) is a birnavirus causing immunosuppressive disease in chickens. Emergence of the very virulent form of IBDV (vvIBDV) in the late 1980s dramatically changed the epidemiology of the disease. In this study, we investigated the phylogenetic origins of its genome segments and estimated the time of emergence of their most recent common ancestors. Moreover, with recently developed coalescence techniques, we reconstructed the past population dynamics of vvIBDV and timed the onset of its expansion to the late 1980s. Our analysis suggests that genome segment A of vvIBDV emerged at least 20 years before its expansion, which argues against the hypothesis that mutation of genome segment A is the major contributing factor in the emergence and expansion of vvIBDV. Alternatively, the phylogeny of genome segment B suggests a possible reassortment event estimated to have taken place around the mid-1980s, which seems to coincide with its expansion within approximately 5 years. We therefore hypothesize that the reassortment of genome segment B initiated vvIBDV expansion in the late 1980s, possibly by enhancing the virulence of the virus synergistically with its existing genome segment A. This report reveals the possible mechanisms leading to the emergence and expansion of vvIBDV, which would certainly provide insights into the scope of surveillance and prevention efforts regarding the disease.

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