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Genus of viruses From Wikipedia, the free encyclopedia
Avibirnavirus is a genus of viruses in family Birnaviridae.[2] There is a single species in this genus: Infectious bursal disease virus, which infects chickens and other fowl. It causes severe inflammation of the bursa of Fabricius, and causes considerable morbidity and mortality.[3][4]
| Avibirnavirus | |
|---|---|
| |
| Infectious bursal disease virus particle | |
Virus classification  | |
| (unranked): | Virus |
| Realm: | Riboviria |
| Kingdom: | Orthornavirae |
| Phylum: | incertae sedis |
| Family: | Birnaviridae |
| Genus: | Avibirnavirus |
| Species[1] | |
Initially, the virus was discovered in 1957 in Gumboro, Delaware, United States.[5][6] Later, the disease was termed Gumboro disease. Since its discovery, the virus has been found to have a worldwide distribution.[6]
Avibirnaviruses are non-enveloped, and their single shelled icosahedral capsid exhibits a T=13 symmetry. The diameter of the capsid is around 70 nm.[3][4]
| Genus | Structure | Symmetry | Capsid | Genomic arrangement | Genomic segmentation |
|---|---|---|---|---|---|
| Avibirnavirus | Icosahedral | T=13 | Non-enveloped | Linear | Segmented |
The double-stranded RNA genome of Avibirnaviruses is linear and segmented into two segments (A and B).[7][8] The combined lengths of the two segments is around 6,000 nucleotides, almost entirely composed of reading-frames. The genome codes for 4-5 proteins depending on the strain.[3][4] The high degree of antigenic variation is due to a combination of high mutation rate and inter-strain homologous recombination within a hypervariable region that is located in the vp2 gene.[6][9]
At approximately 3,200 bp in length, segment A is the larger of the two segments. It contains two partially overlapping open reading frames (ORFs).[7][8] The first ORF in segment A encodes viral protein 5 (VP5).[7] The second ORF in segment A encodes a polyprotein, the pVP2-VP4-VP3 precursor, which is cleaved into three proteins .[7] Segment B encodes a single viral protein, VP1.[7][8]
Viral protein 1 is an RNA-dependent RNA polymerase, which cycles between the two segments and aids in the formation of ribonucleoprotein complexes with viral protein 3.[7]
Viral protein 2 is a major structural component of the virion.[7] The protein contains three domains: base, shell, and projection.[5] The projection domain consists of four loop structures that are exposed on the virion surface.[5] This protein is responsible for inducing a protective immune response, which neutralize monoclonal antibodies through binding to the project domain.[5] The viral protein in conjunction with VP5 acts as an apoptotic inducer, which causes affected cells to become cytotoxic.[9] Also, together with VP5, it inhibits cellular protein synthesis through activation of the protein kinase R pathway (PKR).[9] This activation leads to an increase in reactive oxygen species in the affected cells.[9]
Viral protein 3 is an immunogenic protein that interacts with VP1.[7] Its helps to regulate VP2 apoptosis by inhibiting phosphorylation of PKR and eukaryotic initiation factor 2 (eIF2).[9] Apoptotic regulation allows for the replication and release of the virus into other cells.[9]
Viral protein 4 is a serine protease, which catalyzes the hydrolysis of polyprotein pVP2-VP4-VP3 to release the viral proteins.[7] The serine protease that cleaves at ser-652 and lys-692.[7] This step is essential to replication due to release of the other proteins.[7] VP4 will additionally take over a glucocorticoid-induced leucine zipper protein (GILZ) that will allow for viral growth and block immune response of host cell.[7][9]
Viral protein 5 is an inducer of apoptosis for DF-1 cells.[10] It relies on inhibiting the voltage-dependent anion channel 2 (VDCA2) located on the mitochondria.[10] The inhibition will be aided by VP2, which will close the channel allowing for proliferation of the virus in host cells.[9][10] Also, VDCA2 will bind to RACK1 that will allow replication.[7]
The serotype and antigenic variations of the virus can only be distinguished between through virus-neutralization assays.[5] The project domains can be viewed to see the variation of the virus through amino acid substitutions.[5] The genome is typically highly conserved, however, the serotypes will vary the genome due to nucleotide changes.[8] There are two serotypes of avibirnavirus with one containing multiple classifications.[11] Serotype 1 is pathogenic to chickens especially at 3 to 6 weeks of age and seen to be more virulent in lighter breeds.[11][9] This serotype contains three main classifications: classical virulent IBDV, very virulent IBDV, and variant IBDV.[11][12] Classical virulent IBDV is the only serotype that has two subtypes: attenuated vaccine IBDV and classical virulent IBDV.[12] Although, these serotypes can have variance upon region.[5] Serotype 2 was identified in turkey.[5] This serotype has no pathogenic effect on chickens.[11]
Viral replication is cytoplasmic. Entry into the host cell is achieved by penetration into the host cell. The entry points in the host cell are through certain cell receptors.[11] One receptor that the virus will bind is surface immunoglobulin M, which specifically interacts with the light chains of the antibody.[9] Another receptor that can be bound is heat shock protein 90 (HSP90) on the surface of the DF-1 cell membrane.[9] Although, this receptor will bind either the virus or the VP2-viral sub particle.[9] Entry through the membrane has not been fully understood.[9] The penetration of the membrane is aided by the capsid PEP46.[9] The capid will have a peptide generated from the c-terminal of pVP2 that is released by VP4.[9] The peptide causes the membrane to become permeable by forming pores, which allow for PEP46 entry depending on calcium gradient.[9] If the inner calcium gradient is low, then it is thought to enter V-ATPase positive vesicles by endocytosis and uncoated for entry into the cytosol.[9] Also, it has been found VP2-α4β1 aids in spreading the virus in the cell as well through macropinocytosis.[9] This will allow for the virus to be moved to the early endosomes that is accomplished in the cell through Rab5.[9] Replication follows the double-stranded RNA virus replication model. Double-stranded rna virus transcription is the method of transcription. Young chickens and other fowl serve as the natural host. Transmission routes are contamination.[3][4]
| Genus | Host details | Tissue tropism | Entry details | Release details | Replication site | Assembly site | Transmission |
|---|---|---|---|---|---|---|---|
| Avibirnavirus | Birds | None | Cell receptor endocytosis | Budding | Cytoplasm | Cytoplasm | Contact |
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