Gyrovirus

Gyrovirus is a genus of viruses, in the family Anelloviridae. Until 2011, chicken anemia virus was the only Gyrovirus identified, but since then gyroviruses have also been identified in humans. Diseases associated with this genus include: chicken infectious anemia, which is associated with depletion of cortical thymocytes and erythroblastoid cells.[1][2]

Gyrovirus
Virus classification Edit this classification
(unranked): Virus
Family: Anelloviridae
Genus: Gyrovirus

Taxonomy

The genus contains the following species:[2]

  • Chicken anemia virus
  • Gyrovirus fulga1
  • Gyrovirus galga1
  • Gyrovirus galga2
  • Gyrovirus homsa1
  • Gyrovirus homsa2
  • Gyrovirus homsa3
  • Gyrovirus homsa4
  • Gyrovirus hydho1
  • Gyrovirus myferr1

Structure

Gyroviruses have an average size of 19 to 27 nanometers. They are nonenveloped and have an icosahedral capsid with T=1 symmetry. The unique, single protein, trumpet-shaped capsomeres of Gyrovirus are arranged into 12 pentomers yielding a capsid 60 units in size. The genome is circular, non-segmented, and 2290–2320 nucleotides long.[2][3][4]

GenusStructureSymmetryCapsidGenomic arrangementGenomic segmentation
GyrovirusIcosahedralT=1Non-envelopedCircularMonopartite

Genome

Alignment of the nucleotide sequences of the human gyrovirus genome on the basis of a 138-bp segment (nt 1328–1465) of the viral protein 1 gene. The sequences of the isolate from France (FR823283) and of the 6 isolates found in this http://wwwnc.cdc.gov/eid/article/18/6/12-0179_article.htm study are shown. Nucleotide positions are according to isolate FR823283 (1). Hyphens indicate identity with the prototype sequence of isolate FR823283 (1).

The Gyrovirus genome consists of negative sense, single-stranded, circular, DNA. The genome is relatively small at 2,300 nucleotides. and contains three overlapping open reading frames that code for only three known proteins.[5]

Proteins

The Gyrovirus genome codes for a single polysistronic mRNA that subsequently codes for three proteins, VP1, VP2, and VP3. VP1 is the 51kd capsid protein; in addition to its structural function, it also contains motifs for rolling circle replication in the C-terminal region. VP2 is a 23kd nonstructural protein with phosphatase activity. Virions with mutations in SP2 are still replication competent; however, their cytopathic effects were highly attenuated.[6] VP3, also called apoptin, is a 13kd protein that has been shown to independently induce apoptosis in chicken cells. Apoptin is also being researched for its ability to induce apoptosis in human tumor cells.[7][8]

Replication strategy

Viral replication is nuclear. Entry into the host cell is achieved by penetration into the host cell.[1] Upon entering the host cell, the virus converts from single stranded to double stranded, circular DNA using host cell machinery. The circular dsDNA is then used as a template for transcription and for replication via a rolling circle mechanism similar to phiX174.[9] DNA-templated transcription, with some alternative splicing mechanism is the method of transcription. The virus exits the host cell by nuclear egress, and nuclear pore export. Birds serve as the natural host. Transmission routes are fecal-oral, parental, egg transmission, and respiratory.[1]

GenusHost detailsTissue tropismEntry detailsRelease detailsReplication siteAssembly siteTransmission
GyrovirusBirdsChicken: Thymocytes, erythrobalstoid cells; Egg: embryonal tissues and eggshell membraneCell receptor endocytosisBuddingNucleusNucleusHorizontal: oral-fecal; vertical: bird to egg

Chicken anemia virus

Chicken anemia virus (CAV) was, until 2011, the only member of genus Gyrovirus identified.[10] It causes disease worldwide in areas where chickens are produced. CAV causes severe anemia, hemorrhaging, and depletion of lymphoid tissue through the destruction of bone marrow erythroblastoid cells.[5] The disease affects mainly young chicks not protected by maternal antibodies. Age resistance to disease begins at about one week, but can be overcome however by coinfection with immunosuppressive diseases, such as bursal disease virus, Marek’s disease, and others.[11]

A second virus in this genus—Avian gyrovirus 2—has been described.[12] The viral genome shares ~40% of its sequence with Chicken anemia virus (CAV). The genome is 2383 nucleotides long and has three partially overlapping open reading frames encoding the proteins VP1, VP2 and VP3. These proteins share 38.8%, 40.3%, and 32.2% amino acid identities between their homologs in the CAV.

Two species have been described from humans—human gyrovirus and human gyrovirus 3.[13][14][15] Human gyrovirus 1 appears to be the same virus as avian gyrovirus 2. A fourth gyrovirus—gyrovirus 4 (GyV4)—has been isolated from human stool and chicken meat.[16]

Literature

  1. "Viral Zone". ExPASy. Retrieved 15 June 2015.
  2. "Virus Taxonomy: 2020 Release". International Committee on Taxonomy of Viruses (ICTV). March 2021. Retrieved 23 May 2021.
  3. Crowther, R. A.; et al. (2003). "Comparison of the structures of three circoviruses: Chicken anemia virus, porcine circovirus type 2, and beak and feather disease virus". Journal of Virology. 77 (24): 13036–13041. doi:10.1128/jvi.77.24.13036-13041.2003.
  4. ICTVdB Management (2006). 00.016.0.02. Gyrovirus. In: ICTVdB—The Universal Virus Database, version 4. Büchen-Osmond, C. (Ed), Columbia University, New York, USA.
  5. Noteborn, M.H.M.; et al. "Characterization of Cloned Chicken Anemia Virus DNA That Contains All Elements For The Infectious Replication Cycle". Journal of Virology. 65 (6): 3131–3139.
  6. Peters, Michelle A.; Crabb, Brendan S.; Tivendale, Kelly A.; Browning, Glenn F. (2007). "Attenuation of chicken anemia virus by site-directed mutagenesis of VP2". Journal of General Virology. 88 (8): 2168–2175. doi:10.1099/vir.0.82904-0.
  7. Noteborn, M. H. M.; et al. "A single chicken anemia virus protein induces apoptosis". Journal of Virology. 68 (1): 346–351.
  8. Heckl, Stefan; et al. (2008). "Value of apoptin's 40-amino-acid C-terminal fragment for the differentiation between human tumor and non-tumor cells". Apoptosis. 13 (4): 495–508. doi:10.1007/s10495-007-0174-5.
  9. Noteborn, Mathieu H. M.; Koch, Guus (1995). "Chicken anaemia virus infection: Molecular basis of pathogenicity". Avian Pathology. 24 (1): 11–31. doi:10.1080/03079459508419046.
  10. Phan, T. G.; Li, L.; O'Ryan, M. G.; Cortes, H.; Mamani, N.; Bonkoungou, I. J. O.; Wang, C.; Leutenegger, C. M.; Delwart, E. (14 March 2012). "A third gyrovirus species in human faeces". Journal of General Virology. 93 (Pt_6): 1356–1361. doi:10.1099/vir.0.041731-0. PMC 3755516. PMID 22422066.
  11. Merck Veterinary Manual (online) Accessed 4/20/2009 Chicken Anemia Virus Infection: Introduction http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/200200.htm&word=chicken%2canemia%2cvirus
  12. Rijsewijk, FA; Dos Santos, HF; Teixeira, TF; Cibulski, SP; Varela, AP; Dezen, D; Franco, AC; Roehe, PM (2011). "Discovery of a genome of a distant relative of chicken anemia virus reveals a new member of the genus Gyrovirus". Arch Virol. 156: 1097–1100. doi:10.1007/s00705-011-0971-6.
  13. Sauvage, V; Cheval, J; Foulongne, V; Gouilh, MA; Pariente, K; Manuguerra, JC; Richardson, J; Dereure, O; Lecuit, M; Burguiere, A; Caro, V; Eloit, M (2011). "Identification of the first human gyrovirus, a virus related to chicken anemia virus". J Virol. 85 (15): 7948–7950. doi:10.1128/jvi.00639-11. PMC 3147908.
  14. Maggi, F; Macera, L; Focosi, D; Vatteroni, ML; Boggi, U; Antonelli, G; Eloit, M; Pistello, M (2012). "Human gyrovirus DNA in human blood, Italy". Emerg Infect Dis. 18 (6): 956–9. doi:10.3201/eid1806.120179. PMC 3358173.
  15. Phan, TG; Li, L; O'Ryan, MG; Cortes, H; Mamani, N; Bonkoungou, IJ; Wang, C; Leutenegger, CM; Delwart, E (2012). "A third gyrovirus species in human faeces". J Gen Virol. 93 (6): 1356–1361.
  16. Chu, DK; Poon, LL; Chiu, SS; Chan, KH; Ng, EM; Bauer, I; Cheung, TK; Ng, IH; Guan, Y; Wang, D; Peiris, JS (2012). "Characterization of a novel gyrovirus in human stool and chicken meat". J Clin Virol. 55 (3): 209–213. doi:10.1016/j.jcv.2012.07.001. PMC 3449218.
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