Preferred Scientific Name
- infectious bursal disease virus
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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.Last updated: 10 Dec 2021
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Central African Republic||Absent||Jul-Dec-2019|
|Congo, Democratic Republic of the||Absent||Jul-Dec-2019|
|Côte d'Ivoire||Present, Localized||Jul-Dec-2019|
|Saint Helena||Absent, No presence record(s)||Jan-Jun-2019|
|São Tomé and Príncipe||Present||Jul-Dec-2019|
|Georgia||Absent, No presence record(s)||Jul-Dec-2019|
|-Andaman and Nicobar Islands||Present|
|-Peninsular Malaysia||Present, Serological evidence and/or isolation of the agent|
|Maldives||Absent, No presence record(s)||Jan-Jun-2019|
|Mongolia||Absent, No presence record(s)||Jan-Jun-2019|
|United Arab Emirates||Absent||Jul-Dec-2020|
|Bosnia and Herzegovina||Absent||Jul-Dec-2019|
|Faroe Islands||Absent, No presence record(s)||Jul-Dec-2018|
|Jersey||Absent, No presence record(s)|
|Luxembourg||Absent, No presence record(s)|
|San Marino||Absent, No presence record(s)||Jan-Jun-2019|
|Serbia and Montenegro||Present|
|Bahamas||Absent, No presence record(s)||Jul-Dec-2018|
|Bermuda||Absent, No presence record(s)|
|British Virgin Islands||Absent, No presence record(s)|
|Dominica||Absent, No presence record(s)|
|Greenland||Absent, No presence record(s)||Jul-Dec-2018|
|Saint Kitts and Nevis||Absent, No presence record(s)|
|Saint Vincent and the Grenadines||Absent||Jan-Jun-2019|
|Trinidad and Tobago||Absent||Jan-Jun-2018|
|Federated States of Micronesia||Absent, No presence record(s)||Jan-Jun-2019|
|Marshall Islands||Absent, No presence record(s)||Jan-Jun-2019|
|Falkland Islands||Absent, No presence record(s)||Jul-Dec-2019|
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
|Large segment A||3400||2||polyprotein||110||VP2b*||40-45|
|Small segment B||2800||1||VP1||90|
* VP2b is formed after processing of the 45-50 kDa VP2a precursor protein (van den Berg, 2000).
The function of the different proteins are:
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).
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.
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).
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.
|Animal name||Context||Life stage||System|
|Anser (geese)||Domesticated host|
|Gallus gallus domesticus (chickens)||Domesticated host|
|Meleagris gallopavo (turkey)|
|Muscovy duck||Domesticated host|
|Numida meleagris (guineafowl)|
|Pekin duck||Domesticated host|
|Phasianus colchicus (common pheasant)|
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.
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.
CABI Data Mining, 2001. CAB Abstracts Data Mining.,
CABI, Undated. CABI Compendium: Status inferred from regional distribution. Wallingford, UK: CABI
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (dataset for 2004)., Paris, France: Office International des Epizooties.
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