Borna disease virus

Source: Wikipedia, the free encyclopedia.
Mammalian 1 orthobornavirus
Virus classification Edit this classification
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum:
Negarnaviricota
Class: Monjiviricetes
Order: Mononegavirales
Family: Bornaviridae
Genus: Orthobornavirus
Species:
Mammalian 1 orthobornavirus
Borna disease virus 1 G protein
Identifiers
SymbolBDV_G
PfamPF06208
InterProIPR009344
Available protein structures:
Pfam  structures / ECOD  
PDBRCSB PDB; PDBe; PDBj
PDBsumstructure summary
Borna disease virus 1 P10 protein
Identifiers
SymbolBDV_P10
PfamPF06515
InterProIPR009485
Available protein structures:
Pfam  structures / ECOD  
PDBRCSB PDB; PDBe; PDBj
PDBsumstructure summary
Borna disease virus 1 P40 protein
SCOP2
1n93 / SCOPe / SUPFAM
Available protein structures:
Pfam  structures / ECOD  
PDBRCSB PDB; PDBe; PDBj
PDBsumstructure summary
Borna disease virus 1 P24 protein
Identifiers
SymbolBDV_P24
PfamPF06595
InterProIPR009517
Available protein structures:
Pfam  structures / ECOD  
PDBRCSB PDB; PDBe; PDBj
PDBsumstructure summary

The Borna disease viruses 1 and 2 (BoDV-1 and BoDV-2) are members of the species Mammalian 1 orthobornavirus and cause Borna disease in mammals.

Virology

Genome

BoDV-1/2 have the smallest genome (8.9 kilobases) of any Mononegavirales member and are unique within that order in their ability to replicate within the host cell nucleus.

BoDV-1 was isolated from a diseased horse in the 1970s, but the virus particles were difficult to characterise. Nonetheless, the virus' genome has been characterised. It is a linear negative-sense single stranded RNA virus in the order Mononegavirales.

Several of the proteins encoded by the BoDV-1 genome have been characterised. The G glycoprotein is important for viral entry into the host cell.[1][2]

It has been suggested that the p10, or X, protein plays a role in

ribonucleoprotein transport.[3]

The P40 nucleoprotein from BoDV-1 is multi-helical in

structure and can be divided into two subdomains, each of which has an alpha-bundle topology.[4] The nucleoprotein assembles into a planar homotetramer, with the RNA genome either wrapping around the outside of the tetramer or possibly fitting within the charged central channel of the tetramer
.

P24 (phosphoprotein 24) is an essential component of the RNA

psychiatric diseases
remains alive.

Replication

Bornaviruses enter host cells by

endosome membrane.[10] Replication of bornaviruses occurs inside the nucleus. These are the only animal viruses within the order Mononegavirales to do this. Many plant rhabdoviruses
replicate in the nucleus.

Bornaviruses have negative sense

genomes[11] The negative sense RNA is copied to make a positive sense RNA template. This template is then used to synthesise many copies of the negative sense RNA genome
. This is like making copies of a mold, and then using these molds to make many more viruses.

Endogenous provirus

Endogenous viral elements homologous to the nucleoprotein gene of BoDV-1 have been shown to exist in the genomes of several mammalian species, including humans and non-human primates.[12]

Evolution

A Bayesian analysis of Borna disease virus 1 suggests that the current strains diversified ~300 years ago and that avian-host bornaviruses evolved considerably earlier than this.[13] The ancestral virus seems likely to have been a high AT content virus.

History

Borna disease was first described in 1885 as "heated head disease" of cavalry horses in 1885 in the town of Borna, Germany.[14]

References

  1. PMID 8985354
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  7. ^ .
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  10. ^ Schwemmle, M. and Lipkin, W.I. (2004) Models and mechanisms of Bornavirus pathogenesis. Drug Discovery Today: Disease Mechanisms 1(2):211–216
  11. PMID 11932200
    .
  12. .
  13. .
  14. ^ "Evolutionary Surprise: Eight Percent of Human Genetic Material Comes from a Virus". ScienceDaily. 2010-01-08.

External links