Virus classification
Group: Group IV ((+)ssRNA)
Family: Togaviridae

Togaviridae is a family of viruses. Humans, mammals, birds, and mosquitoes serve as natural hosts. There are currently 32 species in this family, divided among 2 genera. Diseases associated with this family include: Alphaviruses: arthritis, encephalitis; Rubiviruses: rubella.[1][2]


Group: ssRNA(+)



The Togaviridae family belong to group IV of the Baltimore classification of viruses. The genome is linear, non-segmented, single-stranded, positive sense RNA that is 10,000–12,000 nucleotides long. The 5'-terminus carries a methylated nucleotide cap and the 3'-terminus has a polyadenylated tail, therefore resembling cellular mRNA. The virus is enveloped and forms spherical particles (65–70 nm diameter), the capsid within is icosahedral, constructed of 240 monomers, having a triangulation number of 4.[1][3][4]

Genus Structure Symmetry Capsid Genomic Arrangement Genomic Segmentation

Life Cycle

Entry into the host cell is achieved by attachment of the viral E glycoprotein to host receptors, which mediates clathrin-mediated endocytosis.[1] The receptors for binding are unknown, however the tropism is varied and it is known that the glycoprotein petal-like spikes act as attachment proteins. After virus attachment and entry into the cell, gene expression and replication takes place within the cytoplasm.[3][4]

Replication follows the positive stranded RNA virus replication model. Positive-stranded RNA-virus-transcription is the method of transcription. Translation takes place by viral initiation, and suppression of termination. The vector for Togaviridae is primarily the mosquito, where replication of the virus occurs. The Togaviridae family is classified into Old World and New World viruses based on geographical distribution, although it’s likely that a few transoceanic crossings have occurred.[3][4] Human, mammals, marsupials, birds, and mosquitoes serve as the natural host. Transmission routes are zoonosis, bite, and respiratory.[1]

Genus Host Details Tissue Tropism Entry Details Release Details Replication Site Assembly Site Transmission
AlphavirusHumans; mammals; marsupials; birds; mosquitoesNoneClathrin-mediated endocytosisSecretionCytoplasmCytoplasmZoonosis: arthropod bite
RubivirusHumansNoneClathrin-mediated endocytosisSecretionCytoplasmCytoplasmAerosol


The non-structural proteins are encoded at the 5’ end, formed during the first of two characteristic rounds of translation. These proteins are originally translated as a polyprotein, which consequently undergo self cleavage, forming four non-structural proteins responsible for gene expression and replication. The formation of a sub-genomic fragment, encoding the structural proteins and a negative sense fragment, a template for further synthesis of positive sense RNA are the characteristic second phase of translation. Assembly takes place at the cell surface, where the virus buds from the cell, acquiring the envelope. The replication cycle is very fast, taking around 4 hours.[3][4]


Initially the Togavirus family included what are now called the Flaviviruses, within the Alphavirus genus. The Flaviviruses were formed into their own family when sufficient differences with the Alphaviruses were noted thanks to the development of sequencing.[3]


  1. 1 2 3 4 "Viral Zone". ExPASy. Retrieved 15 June 2015.
  2. 1 2 ICTV. "Virus Taxonomy: 2014 Release". Retrieved 15 June 2015.
  3. 1 2 3 4 5 "Togaviridae".
  4. 1 2 3 4 Murray; et al. (2005). Medical Microbiology (5 ed.). Philadelphia: Elsevier Mosby. ISBN 0-323-03325-3.
  5. "Aedes vigilax". NSW Arbovirus Surveillance & Vector Monitoring Program. The New South Wales Arbovirus Surveillance and Mosquito Monitoring Program. Retrieved 2010-06-05. Note that 'Ochlerotatus vigilax' prior to 2000, was known as 'Aedes vigilax'
  6. Doherty, R. L.; Carley, J. G.; Best, J. C. (1972). "Isolation of Ross River virus from man". The Medical journal of Australia. 1 (21): 1083–1084. PMID 5040017.
  7. Meissner, H. C.; Reef, S. E.; Cochi, S. (2006). "Elimination of Rubella from the United States: A Milestone on the Road to Global Elimination". Pediatrics. 117 (3): 933–935. doi:10.1542/peds.2005-1760. PMID 16510677.
  8. Calisher, C. H. (1994). "Medically important arboviruses of the United States and Canada". Clinical Microbiology Reviews. 7 (1): 89–116. PMC 358307Freely accessible. PMID 8118792.
  9. Boughton, C. R.; Hawkes, R. A.; Naim, H. M. (1988). "Illness caused by a Barmah Forest-like virus in New South Wales". The Medical journal of Australia. 148 (3): 146–147. PMID 2828896.
  10. Tsetsarkin, K.; Higgs, S.; McGee, C. E.; Lamballerie, X. D.; Charrel, R. N.; Vanlandingham, D. L. (2006). "Infectious Clones of Chikungunya Virus (La Réunion Isolate) for Vector Competence Studies". Vector-Borne and Zoonotic Diseases. 6 (4): 325–337. doi:10.1089/vbz.2006.6.325. PMID 17187566.
  11. Lahariya, C.; Pradhan, S. K. (2006). "Emergence of chikungunya virus in Indian subcontinent after 32 years: A review". Journal of vector borne diseases. 43 (4): 151–160. PMID 17175699.
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