Psittacine beak and feather disease (PBFD) is a viral disease affecting all Old World and New World parrots. The causative virus—beak and feather disease virus (BFDV)—belongs to the taxonomic genus Circovirus, family Circoviridae. It attacks the feather follicles and the beak and claw matrices of the bird, causing progressive feather, claw and beak malformation and necrosis. In later stages of the disease, feather shaft constriction occurs, hampering development until eventually all feather growth stops. It occurs in an acutely fatal form and a chronic form. Cracking and peeling of the outer layers of the claws and beak make tissues vulnerable to secondary infection. Because the virus also affects the thymus and Bursa of Fabricius, slowing lymphocyte production, immunosuppression occurs, which also means the bird becomes more vulnerable to secondary infections. Beak fractures and necrosis of the hard palate can prevent the bird from eating.
History Psittacine beak and feather disease was first described in the early 1980s and has become recognised as the dominant viral pathogen of psittacine birds worldwide. In wild red-rumped grass parakeets (Psephotus haematonotus), a case of feather loss syndrome, that was highly suggestive of PBFD, was first recorded in South Australia in 1907. The virus causing PBFD was initially designated as psittacine circovirus but has since been renamed beak and feather disease virus (BFDV). The condition is more prevalent in widely occurring Australian species such as the sulphur-crested cockatoo, little corella and galah. The first case of chronic PBFD was reported by Ross Perry in a Control and Therapy article in 1972 for the University of Sydney, in which he described it as "beak rot in a cockatoo". Dr. Perry subsequently studied the disease and wrote extensively about its clinical features in a range of psittacine birds in a long article in which he named the disease "psittacine beak and feather disease syndrome" (PBFDS). This soon became known as psittacine beak and feather disease (PBFD). Earlier observations of what may have been PBFD were recorded in 1888 by the ornithologist Edwin Ashby, observing a flock of completely featherless red-rumped parrots (Psephotus haematonotus) in the Adelaide Hills, South Australia. The species then disappeared from the area for several years.
Beak and feather disease virus PBFD is caused by the beak and feather disease virus (BFDV), a circular or icosahedral, 14–16 nm (1.4×10−5–1.6×10−5 mm) diameter, single-stranded circular DNA, non-enveloped virus with a genome size of between 1992 and 2018 nucleotides. It encodes seven open reading frames—three in the virion strand and four in the complementary strand. The open reading frames have some homology to porcine circovirus (family Circoviridae), subterranean clover stunt virus and faba bean necrotic yellows virus (both family Nanoviridae).
History BFDV was first isolated and characterized by researchers Dr. David Pass of Murdoch University in Perth and Dr. Ross Perry from Sydney, with later work at the University of Georgia in the United States, the University of Sydney and Murdoch University in Australia, and the University of Cape Town, among other centres. The virus was originally designated PCV (psittacine circovirus), but has since been renamed beak and feather disease virus. This is due in part, to the research confirming that this virus is the cause of the disease, and in part to avoid confusion with Porcine circovirus, also called PCV.
Detection A variety of tests for the presence of BFDV are available: standard polymerase chain reaction (PCR), quantitative PCR (qPCR) which can detect the virus in extremely small quantities, whole-genome sequencing, histology, immunohistochemical tests, and quantitative haemagglutination assays.
Structure
The beak and feather disease virus (BFDV) is currently considered a member of the family Circoviridae. Like other circoviruses, BFDV possesses a small, circular single-stranded DNA (ssDNA) genome (approximately 2.0 kb in length) that is encapsidated into a non-enveloped, spherical icosahedral virion. In order to replicate its genome, BFDV needs to invade the nucleus to access the transcriptional machinery of the host cell. The replication of BFDV is known to occur in numerous tissues, including skin, liver, gastrointestinal tract, and bursa of Fabricius; while the capsid antigen of BFDV is found in the spleen, thymus, thyroid, parathyroid and bone marrow. However, the distinction between viral entry and replication in a host cell remains unclear in the absence of confirmation in suitable cell culture. Viral attachment and entry into host cells may not necessarily lead to viral replication, and consequently not all cells containing viral particles may contribute to the disease progression. However, it is thought that the BFDV encodes proteins that actively transport the viral genome into the nucleus, as well as factors that direct the precursor DNA exit to the cytoplasm, where it causes large globular intracytoplasmic paracrystalline arrays. The BFDV genome is bi-directionally transcribed and encodes at least two major proteins: a replication initiation protein (rep) expressed from the virion strand and a capsid protein (cap) expressed from the complementary strand. A recent study conducted by Sarker et al. used a combination of X-ray crystallography, cryo-electron microscopy and atomic force microscopy to investigate the functionality of cap and its interaction with a range of host and viral proteins. They confirmed that the cap protein forms virus-like particles (VLPs) of ~17 nm (mature form) and a smaller assembly of ~10 nm (immature form). Furthermore, this study demonstrated that assembly of these two VLPs is regulated by single-stranded DNA (ssDNA), and that they provide a structural basis of capsid assembly around single-stranded DNA.
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