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Molecular Epidemiology of Oropouche Virus | CDC EID
EID Journal Home > Volume 17, Number 5–May 2011
Volume 17, Number 5–May 2011
Molecular Epidemiology of Oropouche Virus, Brazil
Helena Baldez Vasconcelos, Márcio R.T. Nunes, Lívia M.N. Casseb, Valéria L. Carvalho, Eliana V. Pinto da Silva, Mayra Silva, Samir M.M. Casseb, and Pedro F.C. Vasconcelos
Author affiliations: Instituto Evandro Chagas, Ananindeua, Brazil (H. Baldez Vasconcelos, M.R.T. Nunes, L.M.N. Casseb, V.L. Carvalho, E.V. Pinto da Silva, M. Silva, S.M.M. Casseb, P.F.C. Vasconcelos); and Universidade do Estado do Pará, Belém, Brazil (P.F.C. Vasconcelos)
Suggested citation for this article
Oropouche virus (OROV) is the causative agent of Oropouche fever, an urban febrile arboviral disease widespread in South America, with >30 epidemics reported in Brazil and other Latin American countries during 1960–2009. To describe the molecular epidemiology of OROV, we analyzed the entire N gene sequences (small RNA) of 66 strains and 35 partial Gn (medium RNA) and large RNA gene sequences. Distinct patterns of OROV strain clustered according to N, Gn, and large gene sequences, which suggests that each RNA segment had a different evolutionary history and that the classification in genotypes must consider the genetic information for all genetic segments. Finally, time-scale analysis based on the N gene showed that OROV emerged in Brazil ≈223 years ago and that genotype I (based on N gene data) was responsible for the emergence of all other genotypes and for virus dispersal.
Oropouche virus (OROV) is one of the most common orthobunyaviruses (family Bunyaviridae, genus Orthobunyavirus) (1) and is the causative agent of Oropouche fever in humans, which is clinically characterized as an acute febrile disease (2). The first isolation of OROV was reported in Trinidad and Tobago in 1955, when the virus was isolated from the blood of a febrile patient and from a pool of Coquillettidia venezuelensis mosquitoes (3). OROV was described in Brazil in 1960, when it was isolated from a sloth (Bradypus tridactylus) captured near a forested area during construction of the Belem–Brasilia highway and from a pool of Ochlerotatus (Ochlerotatus) serratus mosquitoes, captured near the same site (4).
Since the first isolation of OROV, >30 outbreaks have been reported in Brazil, Peru, Panama, and Trinidad and Tobago during 1960–2009. At least half a million persons are estimated to have been infected (5,6).
Similar to the genomes of other orthobunyaviruses, the OROV genome comprises 3 single-stranded negative-sense RNA segments—large, medium, and small. The large RNA segment encodes a large protein that has RNA polymerase activity for transcription and replication of genomic RNA segments. The medium segment encodes a precursor polyprotein, which gives rise to the viral surface glycoproteins (Gc and Gn) and to a nonstructural protein NSM. The small RNA encodes a structural nucleocapsid (N) protein, as well as a smaller nonstructural protein (NSS) in overlapping reading frames (1). Studies of the molecular biology of the OROV small RNA segment have suggested its monophyletic origin and the existence of at least 3 genotypes (I, II, and III) (7). Recently, genotype III was isolated from a wild vertebrate host (Callithrix sp.) in southeastern Brazil, suggesting possible dispersion of the virus to susceptible and populated areas in Brazil (8). Further molecular analyses that used OROV strains recovered during outbreaks in Pará State during 2003–2007 demonstrated the association of at least 2 different genotypes (I and II) with Oropouche fever cases in the area (9,10).
In this study, we describe new information regarding the molecular epidemiology of OROV. This information will help clarify the evolution, dispersal, and genotyping classification of this human pathogen in the Brazilian Amazon region.
Suggested Citation for this Article
Baldez Vasconcelos H, Nunes MRT, Casseb LMN, Carvalho VL, Pinto da Silva EV, Silva M, et al. Molecular epidemiology of Oropouche virus, Brazil. Emerg Infect Dis [serial on the Internet]. 2011 May [date cited]. http://www.cdc.gov/EID/content/17/5/800.htm
Comments to the Authors
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Pedro F.C. Vasconcelos, Instituto Evandro Chagas, Rodovia BR-316, KM 7, CEP 66030-000, Ananindeua, Pará, Brazil; email: email@example.com
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