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Rotavirus TEM B82-0337 lores.jpg
Intact double-shelled Rotavirus particles
Virus classification
Group: Group III (dsRNA)
Order: Unassigned
Family: Reoviridae

Reoviridae is a family of viruses that can affect the gastrointestinal system (such as Rotavirus) and respiratory tract. Viruses in the family Reoviridae have genomes consisting of segmented, double-stranded RNA (dsRNA).[1] The name "Reo-" is derived from respiratory enteric orphan viruses.[2] The term "orphan virus" refers to the fact that some of these viruses have been observed not associated with any known disease. Even though viruses in the Reoviridae family have more recently been identified with various diseases, the original name is still used.

Reovirus infection occurs often in humans, but most cases are mild or subclinical. Rotavirus, however, can cause severe diarrhea and intestinal distress in children. The virus can be readily detected in feces, and may also be recovered from pharyngeal or nasal secretions, urine, cerebrospinal fluid, and blood. Despite the ease of finding Reovirus in clinical specimens, their role in human disease or treatment is still uncertain.

Some viruses of this family infect plants. For example, Phytoreovirus and Oryzavirus.


Reoviruses are non-enveloped and have an icosahedral capsid (T-13) composed of an outer and inner protein shell.[2] The genomes of viruses in Reoviridae contain 10–12 segments which are grouped into three categories corresponding to their size: L (large), M (medium) and S (small). Segments range from about 3.9 to 1 kbp and each segment encodes 1–3 proteins. Reoviridae proteins are denoted by the Greek character corresponding to the segment it was translated from (the L segment encodes for λ proteins, the M segment encodes for μ proteins and the S segment encodes for σ proteins).[2]

Since these viruses have dsRNA genomes, replication occurs exclusively in the cytoplasm and the virus encodes several proteins which are needed for replication and conversion of the dsRNA genome into (+)-RNAs. The virus can enter the host cell via a receptor on the cell surface. The receptor is not known but is thought to include sialic acid and junctional adhesion molecules (JAMs).[3] The virus is partially uncoated by proteases in the endolysosome, where the capsid is partially digested to allow further cell entry. The core particle then enters the cytoplasm by a yet unknown process where the genome is transcribed conservatively causing an excess of (+) sense strands, which are used as mRNA templates to synthesize (−) sense strands. Viral particles begin to assemble in the cytoplasm 6–7 hours after infection.

Multiplicity reactivation[edit]

Multiplicity reactivation (MR) is the process by which 2 or more virus genomes, each containing inactivating genome damage, can interact within an infected cell to form a viable virus genome. McClain and Spendlove[4] demonstrated MR for three types of reovirus after exposure to ultraviolet irradiation. In their experiments, reovirus particles were exposed to doses of UV-light that would be lethal in single infections. However, when two or more inactivated viruses were allowed to infect individual host cells MR occurred and viable progeny were produced. As they stated, multiplicity reactivation by definition involves some type of repair. Michod et al.[5] reviewed numerous examples of MR in different viruses, and suggested that MR is a common form of sexual interaction in viruses that provides the benefit of recombinational repair of genome damages.

Genera and type species[edit]

Fifteen genera of the Reoviridae are known and the largest of these genera is the Orbivirus with 22 species and 13 unassigned viruses.

The Reoviridae are divided based on the presence of a "turret" protein on the inner capsid.[6][7]

As of July 2009, ratified by the ICTV, there are two subfamilies; Sedoreovirinae & Spinareovirinae in the family Reoviridae.[8]

"The name Spinareovirinae will be used to identify the subfamily containing the spiked or turreted viruses and is derived from ‘reovirus’ and the Latin word ‘spina’ as a prefix, which means spike, denoting the presence of spikes or turrets on the surface of the core particles. The term ‘spiked’ is an alternative to ‘turreted’, that was used in early research to describe the structure of the particle, particularly with the cypoviruses. The name Sedoreovirinae will be used to identify the subfamily containing the non-turreted virus genera and is derived from ‘reovirus’ and the Latin word ‘sedo’, which means smooth, denoting the absence of spikes or turrets from the core particles of these viruses, which have a relatively smooth morphology."[9]

Phylogenetic comparison of the viral polymerase protein sequences of viruses of the family Reoviridae. Arrow indicates a common phylogenetic origin between seadornaviruses and rotaviruses.

The subfamily Sedoreovirinae contains 6 genera:

The subfamily Spinareovirinae contains 9 genera:

Proposed genera:

Piscine reovirus belongs to an as yet classified genus in the subfamily Spinareovirinae.[11]

Therapeutic applications[edit]

The reoviruses have been demonstrated to have oncolytic (cancer-killing) properties, encouraging the development of reovirus-based therapies for cancer treatment.[12][13]

Reolysin is a formulation of reovirus that is currently in clinical trials for the treatment of various cancers.[14]

See also[edit]


  1. ^ Patton JT (editor). (2008). Segmented Double-stranded RNA Viruses: Structure and Molecular Biology. Caister Academic Press. isbn = 978-1-904455-21-9. 
  2. ^ a b c MicrobiologyBytes—Reoviruses
  3. ^ Barton, ES; Forrest, JC, Connolly, JL, Chappell, JD, Liu, Y, Schnell, FJ, Nusrat, A, Parkos, CA, Dermody, TS (Feb 9, 2001). "Junction adhesion molecule is a receptor for reovirus.". Cell 104 (3): 441–51. doi:10.1016/S0092-8674(01)00231-8. PMID 11239401. 
  4. ^ McClain ME, Spendlove RS (November 1966). "Multiplicity reactivation of reovirus particles after exposure to ultraviolet light". J. Bacteriol. 92 (5): 1422–9. PMC 276440. PMID 5924273. 
  5. ^ Michod, R. E.; Bernstein, H.; Nedelcu, A. M. (2008). "Adaptive value of sex in microbial pathogens". Infection, Genetics and Evolution 8 (3): 267–285. doi:10.1016/j.meegid.2008.01.002. PMID 18295550. 
  6. ^ Hill, Claire; Booth T et al. (1999). "The structure of a cypovirus and the functional organization of dsRNA viruses". Nature Structural Biology 6 (6): 565–9. doi:10.1038/9347. PMID 10360362. 
  7. ^ Knipe, David; Howley P et al. (2006). Fields Virology. Philadelphia, Pa.: Wolters Kluwer, Lippincott Williams & Wilkins. p. 1855. ISBN 0-7817-6060-7. 
  8. ^ Carstens, E. B. (January 2010). "Ratification vote on taxonomic proposals to the International Committee on Taxonomy of Viruses (2009)" (PDF). Archives of Virology 155 (1): 133–146. doi:10.1007/s00705-009-0547-x. PMID 19960211. 
  9. ^ Attoui, Houssam; Mertens, Peter. 2007.127-129V.v2.Spina-Sedoreovirinae. ICTV. pp. 1–9  Missing or empty |title= (help); |chapter= ignored (help)
  10. ^ Deng, X. X.; Lü, L.; Ou, Y. J.; Su, H. J.; Li, G.; Guo, Z. X.; Zhang, R.; Zheng, P. R.; Chen, Y. G.; He, J. G.; Weng, S. P. (2012). "Sequence analysis of 12 genome segments of mud crab reovirus (MCRV)". Virology 422 (2): 185–194. doi:10.1016/j.virol.2011.09.029. PMID 22088215. 
  11. ^ Kibenge MJ, Iwamoto T, Wang Y, Morton A, Godoy MG, Kibenge FS (2013). "Whole-genome analysis of piscine reovirus (PRV) shows PRV represents a new genus in family Reoviridae and its genome segment S1 sequences group it into two separate sub-genotypes". Virol. J. 10: 230. doi:10.1186/1743-422X-10-230. PMC 3711887. PMID 23844948. 
  12. ^ Lal R, Harris D, Postel-Vinay S, de Bono J (October 2009). "Reovirus: Rationale and clinical trial update". Curr. Opin. Mol. Ther. 11 (5): 532–9. PMID 19806501. 
  13. ^ Kelland, K. (13 June 2012). "Cold virus hitches a ride to kill cancer: study". Reuters. Retrieved 17 June 2012. 
  14. ^ Thirukkumaran C, Morris DG (2009). "Oncolytic viral therapy using reovirus". Methods Mol. Biol. Methods in Molecular Biology 542: 607–34. doi:10.1007/978-1-59745-561-9_31. ISBN 978-1-934115-85-5. PMID 19565924. 

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