Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide

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infectious bursal disease virus

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Datasheet

infectious bursal disease virus

Summary

  • Last modified
  • 14 July 2018
  • Datasheet Type(s)
  • Invasive Species
  • Preferred Scientific Name
  • infectious bursal disease virus
  • Taxonomic Tree
  • Domain: Virus
  •   Unknown: "Positive sense ssRNA viruses"
  •     Unknown: "RNA viruses"
  •       Family: Birnaviridae
  •         Genus: Avibirnavirus
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    Compendia
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    OX10 8DE
    UK
    compend@cabi.org
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Identity

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Preferred Scientific Name

  • infectious bursal disease virus

English acronym

  • IBDV

Taxonomic Tree

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  • Domain: Virus
  •     Unknown: "Positive sense ssRNA viruses"
  •         Unknown: "RNA viruses"
  •             Family: Birnaviridae
  •                 Genus: Avibirnavirus
  •                     Species: infectious bursal disease virus

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

AzerbaijanLast reported2002OIE Handistatus, 2005
BahrainSerological evidence and/or isolation of the agentOIE Handistatus, 2005
BhutanReported present or known to be presentOIE Handistatus, 2005
Brunei DarussalamReported present or known to be presentOIE Handistatus, 2005
ChinaPresentCAB ABSTRACTS Data Mining 2001
-Hong KongReported present or known to be presentOIE Handistatus, 2005
Georgia (Republic of)Disease never reportedOIE Handistatus, 2005
IndiaOIE Handistatus, 2005
-Andaman and Nicobar IslandsPresentCAB ABSTRACTS Data Mining 2001
IndonesiaReported present or known to be presentOIE Handistatus, 2005
IranReported present or known to be presentOIE Handistatus, 2005
IraqReported present or known to be presentOIE Handistatus, 2005
IsraelNo information availableOIE Handistatus, 2005
JapanReported present or known to be presentOIE Handistatus, 2005
JordanReported present or known to be presentOIE Handistatus, 2005
KazakhstanDisease not reportedOIE Handistatus, 2005
Korea, DPROIE Handistatus, 2005
Korea, Republic ofReported present or known to be presentOIE Handistatus, 2005
KuwaitLast reported1996OIE Handistatus, 2005
LebanonLast reported2000OIE Handistatus, 2005
MalaysiaPresentPresent based on regional distribution.
-Peninsular MalaysiaSerological evidence and/or isolation of the agentOIE Handistatus, 2005
-SabahLast reported2003OIE Handistatus, 2005
-SarawakReported present or known to be presentOIE Handistatus, 2005
MongoliaDisease never reportedOIE Handistatus, 2005
MyanmarReported present or known to be presentOIE Handistatus, 2005
NepalReported present or known to be presentOIE Handistatus, 2005
OmanReported present or known to be presentOIE Handistatus, 2005
PhilippinesReported present or known to be presentOIE Handistatus, 2005
QatarNo information availableOIE Handistatus, 2005
SingaporeLast reported1986OIE Handistatus, 2005
Sri LankaReported present or known to be presentOIE Handistatus, 2005
SyriaDisease not reportedOIE Handistatus, 2005
TaiwanReported present or known to be presentOIE Handistatus, 2005
TajikistanNo information availableOIE Handistatus, 2005
ThailandReported present or known to be presentOIE Handistatus, 2005
TurkeyLast reported1996OIE Handistatus, 2005
TurkmenistanNo information availableOIE Handistatus, 2005
United Arab EmiratesReported present or known to be presentOIE Handistatus, 2005
UzbekistanLast reported1995OIE Handistatus, 2005
VietnamReported present or known to be presentOIE Handistatus, 2005
YemenNo information availableOIE Handistatus, 2005

Africa

AlgeriaLast reported2003OIE Handistatus, 2005
AngolaReported present or known to be presentOIE Handistatus, 2005
BeninReported present or known to be presentOIE Handistatus, 2005
BotswanaLast reported2002OIE Handistatus, 2005
Burkina FasoReported present or known to be presentOIE Handistatus, 2005
BurundiNo information availableOIE Handistatus, 2005
CameroonReported present or known to be presentOIE Handistatus, 2005
Cape VerdeReported present or known to be presentOIE Handistatus, 2005
Central African RepublicReported present or known to be presentOIE Handistatus, 2005
ChadNo information availableOIE Handistatus, 2005
Congo Democratic RepublicNo information availableOIE Handistatus, 2005
Côte d'IvoireReported present or known to be presentOIE Handistatus, 2005
DjiboutiDisease not reportedOIE Handistatus, 2005
EgyptLast reported1999OIE Handistatus, 2005
EritreaReported present or known to be presentOIE Handistatus, 2005
EthiopiaDisease not reportedOIE Handistatus, 2005
GhanaReported present or known to be presentOIE Handistatus, 2005
Guinea-BissauNo information availableOIE Handistatus, 2005
KenyaReported present or known to be presentOIE Handistatus, 2005
LibyaReported present or known to be presentOIE Handistatus, 2005
MalawiReported present or known to be presentOIE Handistatus, 2005
MaliNo information availableOIE Handistatus, 2005
MauritiusLast reported2001OIE Handistatus, 2005
MoroccoReported present or known to be presentOIE Handistatus, 2005
MozambiqueReported present or known to be presentOIE Handistatus, 2005
NamibiaReported present or known to be presentOIE Handistatus, 2005
NigeriaReported present or known to be presentOIE Handistatus, 2005
RéunionNo information availableOIE Handistatus, 2005
RwandaNo information availableOIE Handistatus, 2005
Sao Tome and PrincipeSerological evidence and/or isolation of the agentOIE Handistatus, 2005
SenegalNo information availableOIE Handistatus, 2005
SeychellesReported present or known to be presentOIE Handistatus, 2005
SomaliaNo information availableOIE Handistatus, 2005
South AfricaReported present or known to be presentOIE Handistatus, 2005
SudanReported present or known to be presentOIE Handistatus, 2005
SwazilandDisease not reportedOIE Handistatus, 2005
TanzaniaReported present or known to be presentOIE Handistatus, 2005
TogoLast reported2003OIE Handistatus, 2005
TunisiaReported present or known to be presentOIE Handistatus, 2005
UgandaReported present or known to be presentOIE Handistatus, 2005
ZambiaReported present or known to be presentOIE Handistatus, 2005
ZimbabweReported present or known to be presentOIE Handistatus, 2005

North America

BermudaDisease not reportedOIE Handistatus, 2005
CanadaReported present or known to be presentOIE Handistatus, 2005
MexicoReported present or known to be presentOIE Handistatus, 2005
USAReported present or known to be presentOIE Handistatus, 2005

Central America and Caribbean

BarbadosReported present or known to be presentOIE Handistatus, 2005
BelizeNo information availableOIE Handistatus, 2005
British Virgin IslandsDisease never reportedOIE Handistatus, 2005
Cayman IslandsDisease not reportedOIE Handistatus, 2005
Costa RicaNo information availableOIE Handistatus, 2005
CubaReported present or known to be presentOIE Handistatus, 2005
CuraçaoDisease not reportedOIE Handistatus, 2005
DominicaDisease not reportedOIE Handistatus, 2005
Dominican RepublicReported present or known to be presentOIE Handistatus, 2005
El SalvadorNo information availableOIE Handistatus, 2005
GuadeloupeNo information availableOIE Handistatus, 2005
GuatemalaNo information availableOIE Handistatus, 2005
HaitiReported present or known to be presentOIE Handistatus, 2005
HondurasReported present or known to be presentOIE Handistatus, 2005
JamaicaReported present or known to be presentOIE Handistatus, 2005
MartiniqueReported present or known to be presentOIE Handistatus, 2005
NicaraguaNo information availableOIE Handistatus, 2005
PanamaNo information availableOIE Handistatus, 2005
Saint Kitts and NevisDisease never reportedOIE Handistatus, 2005
Saint Vincent and the GrenadinesNo information availableOIE Handistatus, 2005
Trinidad and TobagoNo information availableOIE Handistatus, 2005

South America

ArgentinaReported present or known to be presentOIE Handistatus, 2005
BoliviaOIE Handistatus, 2005
BrazilReported present or known to be presentOIE Handistatus, 2005
ChileReported present or known to be presentOIE Handistatus, 2005
ColombiaReported present or known to be presentOIE Handistatus, 2005
EcuadorDisease not reportedOIE Handistatus, 2005
Falkland IslandsDisease never reportedOIE Handistatus, 2005
French GuianaDisease not reportedOIE Handistatus, 2005
GuyanaDisease not reportedOIE Handistatus, 2005
ParaguayReported present or known to be presentOIE Handistatus, 2005
PeruReported present or known to be presentOIE Handistatus, 2005
UruguayReported present or known to be presentOIE Handistatus, 2005
VenezuelaReported present or known to be presentOIE Handistatus, 2005

Europe

AndorraNo information availableOIE Handistatus, 2005
AustriaNo information availableOIE Handistatus, 2005
BelarusNo information availableOIE Handistatus, 2005
BelgiumNo information availableOIE Handistatus, 2005
Bosnia-HercegovinaDisease not reportedOIE Handistatus, 2005
BulgariaLast reported1998OIE Handistatus, 2005
CroatiaReported present or known to be presentOIE Handistatus, 2005
CyprusReported present or known to be presentOIE Handistatus, 2005
Czech RepublicDisease not reportedOIE Handistatus, 2005
DenmarkReported present or known to be presentOIE Handistatus, 2005
EstoniaDisease not reportedOIE Handistatus, 2005
FinlandLast reported2003OIE Handistatus, 2005
FranceReported present or known to be presentOIE Handistatus, 2005
GermanyReported present or known to be presentOIE Handistatus, 2005
GreeceOIE Handistatus, 2005
HungaryReported present or known to be presentOIE Handistatus, 2005
IcelandLast reported1998OIE Handistatus, 2005
IrelandReported present or known to be presentOIE Handistatus, 2005
Isle of Man (UK)No information availableOIE Handistatus, 2005
ItalyNo information availableOIE Handistatus, 2005
JerseyDisease not reportedOIE Handistatus, 2005
LatviaLast reported1997OIE Handistatus, 2005
LiechtensteinDisease not reportedOIE Handistatus, 2005
LithuaniaCAB Abstracts data miningOIE Handistatus, 2005
LuxembourgDisease never reportedOIE Handistatus, 2005
MacedoniaReported present or known to be presentOIE Handistatus, 2005
MaltaReported present or known to be presentOIE Handistatus, 2005
MoldovaLast reported1996OIE Handistatus, 2005
NetherlandsReported present or known to be presentOIE Handistatus, 2005
NorwayReported present or known to be presentOIE Handistatus, 2005
PolandLast reported2003OIE Handistatus, 2005
PortugalReported present or known to be presentOIE Handistatus, 2005
RomaniaOIE Handistatus, 2005
Russian FederationReported present or known to be presentOIE Handistatus, 2005
SlovakiaLast reported2003OIE Handistatus, 2005
SloveniaReported present or known to be presentOIE Handistatus, 2005
SpainNo information availableOIE Handistatus, 2005
SwedenLast reported2000OIE Handistatus, 2005
SwitzerlandNo information availableOIE Handistatus, 2005
UKReported present or known to be presentOIE Handistatus, 2005
-Northern IrelandReported present or known to be presentOIE Handistatus, 2005
UkraineLast reported2002OIE Handistatus, 2005
Yugoslavia (former)No information availableOIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro)Reported present or known to be presentOIE Handistatus, 2005

Oceania

AustraliaReported present or known to be presentOIE Handistatus, 2005
French PolynesiaReported present or known to be presentOIE Handistatus, 2005
New CaledoniaReported present or known to be presentOIE Handistatus, 2005
New ZealandLast reported1999OIE Handistatus, 2005
SamoaDisease not reportedOIE Handistatus, 2005
VanuatuLast reported1997OIE Handistatus, 2005
Wallis and Futuna IslandsNo information availableOIE Handistatus, 2005

Pathogen Characteristics

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The virus


Infectious bursal disease virus belongs to the family of Birnaviridae, genus Avibirnavirus.Birnaviruses carry a bisegmented (hence the name bi-RNAviruses) double-stranded RNA genome (Müller et al., 1992; Becht, 1994). The virion is non-enveloped, single-shelled, and negatively stained particles are about 55-65 nm in diameter. The icosahedral capsid is composed of 32 capsomers and includes the viral genome. The structural polypeptides VP2 and VP3 represent the major structural proteins of the virus (McFerran, 1993). The buoyant density of mature infectious particles in CsCl has been reported between 1.31-1.34 g/ml (McFerran, 1993). Lower density values may represent incomplete virus particles (Lukert and Saif, 1991).

The virus is highly stable, and is resistant to ether and chloroform. It remains viable between pH 2- 12, and after incubation at 56°C for 5 hours, or at 60°C for 30 minutes. It is inactivated by heating at 70°C for 30 minutes (McFerran, 1993). Chloramine solution, formalin and mixtures of formaldehyde, gluteraldehyde and alkyl di-methyl-benzyl-ammonium chloride have been reported as suitable disinfectants at specific concentrations or temperatures (McFerran, 1993). As a consequence IBDV can persist in poultry houses even after thorough cleansing and disinfection. The virus has survived in poultry houses for 122 days after removal of infected birds, and in contaminated feed, water and faeces for at least 52 days (McFerran, 1993). Hygienic measures are therefore insufficient to control IBD, and vaccination is necessary to control the disease.

The two RNA segments are designated A and B. The larger segment A, comprised of approximately 3400 base-pairs (bps), contains two open reading frames (ORFs) (Müller et al., 1992; Van den Berg, 2000). The large ORF codes for a single large polyprotein composed of 1012 amino acids, on which the structural capsid proteins VP2 and VP3, and the non-structural protein VP4 are arranged. This polyprotein is cleaved co- or post-translationally (Müller et al., 1992). VP2 is formed in two steps, first as a 45-50 kDa precursor protein VP2a, which is further processed into a smaller VP2b 404-5 kDa protein. Expression of VP2a alone leads to formation of tubule-like structures but not virus-like particles. Segment A can encode for a short 17 kDa protein, VP5, from a partly overlapping ORF (Van den Berg, 2000). This protein may be involved in the induction of virus release and apoptosis (Van den Berg, 2000; Yao and Vakharia, 2001). VP5 is a non-essential protein that is not required for productive replication of IBDV (Mundt et al., 1997).

The smaller segment B, comprising approximately 2800 basepairs encodes VP1 in one single ORF. VP1 is a multifunctional virus enzyme. It is firmly linked to the ends of the two genome segments, and VP1 is associated in this complex with replicase and transferase activities, as well as guanyltransferase and methyltransferase activities (Müller et al., 1992)(see table below).

Table: Viral proteins of IBDV


 bpsORFsproteinskDaproteinkDa
Large segment A34002polyprotein110VP2b*40-45
VP330-32
VP428
VP517
Small segment B28001  VP190

* VP2b is formed after processing of the 45-50 kDa VP2a precursor protein (van den Berg, 2000).

The function of the different proteins are:

  • VP2b- a structural protein, major host-protective immunogen, antigenic variation, tissue trophism and virulence.
  • VP3- a structural protein, a group specific antigen.
  • VP4- A virus encoded protease, auto processing of precursor protein.
  • VP5- Non-structural protein, virus release and may be involved in apotosis.
  • VP1- A viral RNA polymerase.

Recent studies have shown that only expression of the polyprotein gives rise to the formation of virus-like particles (VLPs), with size and shape very similar to those of authentic IBDV particles (Van den Berg, 2000).


Serotypes


Two serotypes of IBDV occur. Serotype I viruses encompass the classical strains causing bursal disease in chicks, and are pathogenic for chickens with selective tropism for lymphoid cells in the Bursa of Fabricius. Serotype II differentiates the non-pathogenic viruses that do not preferentially replicate in the bursa, and which were originally isolated from turkeys. The two serotypes can be differentiated by virus neutralization tests (VNT). Serotype I viruses show broad antigenic variation and have been further subdivided (McFerran, 1993). Evidence for a subdivision is that certain serotype I infected birds are not protected by serotype I vaccines (McFerran, 1993). At least six subtypes have been recognized and are referred to as variant IBD viruses (McFerran, 1993).

Serotype I can be classified as mild, intermediate, intermediate plus (‘hot’), classical, variant or very virulent. The first three classes tend to cause no mortality and mild to severe bursal lesions. The latter three cause increasing mortality and severe bursal lesions. Serotype II is non-virulent and causes no clinical signs. The very virulent IBDV strains belong to classical serotype I viruses, but have a distinct pathology. No virulence markers have yet unambiguously been identified (Nagarjan and Kibenge, 1997).

VP2 is the dominant virus protein involved in binding of neutralizing antibodies, and contains several neutralizing epitopes (Becht, 1994). The corresponding antigenic sites are highly conformation dependent (Becht, 1994).

Serotype I infections in chickens cause clinical disease, but occur sub-clinically in turkeys. Serotype II infections occur sub-clinically in chickens, but infections are uncommon, and its pathogenic potential in turkeys is unclear (Becht, 1994). There is no cross-protection and antibodies against serotype II do not protect against infections with serotype I.


Cell tropism and virus replication


The characteristic cell tropism of IBDV largely defines its pathogenic potential. Serotype I IBDV viruses preferentially replicate in lymphoid cells of the bursa, during specific stages of maturation, in the young bird. Stem cells, or peripheral B-cells, are refractory to IBDV replication. As a consequence, chickens show age-dependent sensitivity for IBDV and lethal infections are mostly restricted to 3-6 weeks of age, when the bursa is in its maximal stage of development (Becht, 1994). However, infections caused by vvIBDVs may occur during the whole growing period of broilers. Furthermore, virus load may be found in non-bursal lymphopoetic organs and haematopoetic organs. A higher frequency of IBDV antigen-positive cells in the thymus, spleen and bone marrow, can be demonstrated after infection of birds with vvIBDV compared with other strains (van den Berg, 2000).

IBDV strains may be cultivated in chicken embryo cells (CEC) and replication of the virus results in cytopathologic effects (CPE) and plaque formation (Becht, 1994). Titres of 107 plaque forming units (PFU) per ml may be reached 12-16 hours after infection.

A typical characteristic of IBDV is that the cellular synthesis of host cell proteins is not shut off during replication, and this hampers research into the replication mechanisms of IBDV (Becht, 1994). This phenomenon may be necessary for the pathogenicity of the virus. It has been demonstrated that cellular molecules interact with virulent IBDV, which may be a pre-requisite for efficient IBDV replication. IBDV was shown to bind to proteins with molecular weights of 70, 82 and 110 kDa in the IBDV-permissive chicken B lymphoblastoid cell line LSCC-BK3, but further characterization of the virus receptor molecules requires more study (Setiyono et al., 2001).

Inoculation of the chorioallantoic membrane (CAM) is the most sensitive route of inoculation for growth of IBDV, and virus titres of 104-106 embryo infectious doses (EID50) per gram are found in the CAM and the embryo (McFerran, 1993). The allantoic sac is the least desirable, yielding EID50 virus titres of 1.5-2 log10 lower than by the CAM route. Mortality starts usually around day 3 post-infection, and all embryos are dead by day 7. Some strains will also grow in chicken embryo fibroblast cells (CEF), chicken embryo bursal and kidney cells, turkey and duck embryo cells, RK13 (a transformed rabbit kidney cell), MDBK (Madin Darby Bovine Kidney), BSC-1 (Monkey kidney cells), and Vero (African green monkey) cells (McFerran, 1993).

The B-cell lines LSCC-BK3 and LSCC-CU10 are susceptible to both virulent and avirulent strains, whilst the LSCC-1104-B-1 line is susceptible only to the attenuated IBDV, and peak titres are reached 72 hours post-infection (McFerran, 1993). The virus does not show haemagglutinating activity (McFerran, 1993).


Virulence


Although extensive research on the antigenic variation of the VP2 protein has been performed, no definitive hot spot has been identified that determines the virulence. Re-assortant IBDV strains that possessed segment A of the virulent IBDV serotype 1 Cu-1 and segment B of the serotype 2 strain 23/82, showed that virulence could not be attributed to one of the segments alone. Both segments contribute to the replication in the Bursa of Fabricius. Thus, replication of IBDV is controlled by the interaction of genomic products from both RNA segments, and not by products of one segment alone. The virulence of IBDV appears to be multigenic (Müller et al., 1992, van den Berg, 2000). While continuous natural passage from bird to bird fully maintains the pathogenic capacity of the virus, IBDV strains typically loose their pathogenicity after a single replication cycle in vitro (Becht, 1994). However, the virus replication in the Bursa Fabricius is not depressed and leads to severe depletion of follicles, although not coinciding with clinical signs (Becht, 1994). Information is available on the genetic characterization of IBDV attenuation. It has been shown that five successive passages of two attenuated IBDV strains (used as commercial live vaccine) in specific- pathogen-free chickens resulted in increased virulence during the passage in susceptible chickens, as evidenced by a decrease in Bursa:body weight ratios. A direct nucleotide sequence analysis of the VP2 hypervariable domain amplified by the reverse transcription-polymerase chain reaction, revealed that the nucleotide at position 890 (T) in both strains was A after the passage in chicken. In addition, the nucleotide at position 890 (A) was T or C after the subsequent passage in CEF cells .

Disease(s) associated with this pathogen is/are on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's Handistatus database on disease occurrence. Please see the AHPC library for further information from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.

Vectors and Intermediate Hosts

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VectorSourceReferenceGroupDistribution
Alphitobius diaperinusNematode

References

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Abdel-Alim GA; Saif YM, 2001. Immunogenicity and antigenicity of very virulent strains of infectious bursal disease viruses. Avian Dis., 45:92-101.

Becht H, 1994. Birnaviruses - Animal. In: Webster RG, Garnoff A, eds. Encyclopedia of virology Vol. 1. London, UK: Academic Press, Harcourt Brace & Company, 143-149.

Lukert PD; Saif YM, 1991. Infectious bursal disease. Diseases of poultry., ed. 9:648-663; 145 ref.

McFerran JB, 1993. Infectious bursal disease. Virus infections of birds., 213-228; 84 ref.

Mundt E; Köllner B; Kretzschmar D, 1997. VP5 of infectious bursal disease virus is not essential for viral replication in cell culture. Journal of Virology, 71(7):5647-5651; 15 ref.

Müller H et al., 1992. Infectious bursal disease virus of poultry: antigenic structure of the virus and control. Veterinary Microbiology, 33:175-183.

Nagarajan MM; Kibenge FSB, 1997. Infectious bursal disease virus: a review of molecular basis for variations in antigenicity and virulence. Canadian Journal of Veterinary Research, 61(2):81-88; 75 ref.

OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.

OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.

OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.

OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.

Setiyono A et al., 2001. Isolation of monoclonal antibodies that inhibit the binding of infectious bursal disease virus to LSCC-BK3 cells. Journal of Veterinary Medical Science, 63(2):215-218.

van den Berg TP, 2000. Acute infectious bursal disease in poultry: a review. Avian Pathol., 29:175-194.

Yao K; Vakharia VN, 2001. Induction of apoptosis in vitro by the 17 -kDa nonstructural protein of infectious bursal disease virus: possible role in viral pathogenesis. Virology, 285:50-58.

Distribution Maps

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