Sindbis virus

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Sindbis virus
CryoEM model of Sindbis virus. EMDB entry EMD-2374[1]
Virus classification e
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Kitrinoviricota
Class: Alsuviricetes
Order: Martellivirales
Family: Togaviridae
Genus: Alphavirus
Sindbis virus

Sindbis virus (SINV) is a member of the Togaviridae family, in the Alphavirus genus. The virus was first isolated in 1952 in Cairo, Egypt.[2] The virus is transmitted by mosquitoes (Culex spp.) SINV causes sindbis fever in humans and the symptoms include arthralgia, rash and malaise. Sindbis fever is most common in Southern Africa, East Africa, Egypt, Palestine, the Philippines and parts of Australia.

It is an arbovirus, meaning that it is arthropod-borne, and is maintained in nature by transmission between vertebrate (bird) hosts and invertebrate (mosquito) vectors. Humans are infected with Sindbis virus when bitten by an infected mosquito. SINV has been linked to Pogosta disease in Finland,[3] Ockelbo disease in Sweden and Karelian fever in Russia.

Virus physiology[edit]

Structure, genome & replication Sindbis viruses are enveloped particles with an icosahedral capsid. Its genome is a positive single stranded RNA approximately 11.7kb long. It has a 5' cap and 3' polyadenylated tail therefore serves directly as messenger RNA (mRNA) in a host cell. The genome encodes four non-structural proteins at the 5' end and the capsid and two envelope proteins at the 3' end. This is characteristic of all Togaviruses. Replication is cytoplasmic and rapid. The genomic RNA is partially translated at the 5’ end to produce the non-structural proteins which are then involved in genome replication and the production of new genomic RNA and a shorter sub-genomic RNA strand. This sub-genomic strand is translated into the structural proteins. The viruses assemble at the host cell surfaces and acquire their envelope through budding.

A non-coding RNA element has been found to be essential for Sindbis virus genome replication.[4]

Recombination has been demonstrated between RNAs of Sindbis virus.[5][6] The mechanism of recombination appears to be template switching (copy choice) during RNA replication.[5][6]

See also[edit]


  1. ^ Cao, S.; Zhang, W. (2013). "Characterization of an early-stage fusion intermediate of Sindbis virus using cryoelectron microscopy". Proceedings of the National Academy of Sciences. 110 (33): 13362–13367. Bibcode:2013PNAS..11013362C. doi:10.1073/pnas.1301911110. PMC 3746934. PMID 23898184.
  2. ^ Ling J, Smura T, Lundström JO, Pettersson JH, Sironen T, Vapalahti O, Lundkvist Å, Hesson JC (30 July 2019). "Introduction and Dispersal of Sindbis Virus from Central Africa to Europe". J Virol. 93 (16): e00620-19. doi:10.1128/JVI.00620-19. PMC 6675900. PMID 31142666.
  3. ^ Kurkela S, Manni T, Vaheri A, Vapalahti O. Causative agent of Pogosta disease isolated from blood and skin lesions, Emerg Infect Dis [serial on the Internet]. Published 2004 May. (accessed 2007-10-16)
  4. ^ Frolov, I; Hardy R; Rice CM (2001). "Cis-acting RNA elements at the 5' end of Sindbis virus genome RNA regulate minus- and plus-strand RNA synthesis". RNA. 7 (11): 1638–1651. doi:10.1017/S135583820101010X. PMC 1370205. PMID 11720292.
  5. ^ a b Lai MM. RNA recombination in animal and plant viruses. Microbiol Rev. 1992 Mar;56(1):61-79. PMID: 1579113; PMCID: PMC372854
  6. ^ a b Weiss BG, Schlesinger S. Recombination between Sindbis virus RNAs. J Virol. 1991 Aug;65(8):4017-25. doi: 10.1128/JVI.65.8.4017-4025.1991. PMID: 2072444; PMCID: PMC248832

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