Complete sequence of the genomic RNA of O'Nyong-Nyong virus and its use in the construction of alphavirus phylogenetic trees

Levinson, Randy; Strauss, James H.; Strauss, Ellen G.

doi:10.1016/0042-6822(90)90191-s

Cited by 114 publications

(85 citation statements)

References 25 publications

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“…(Hahn et al, 1988). Comparisons using the amino acid sequences of several alphaviruses has confirmed that the envelope glycoproteins were derived from the SINVlike ancestor, whilst the capsid protein was derived from the EEEV-like ancestor (Levinson et al, 1990). Further phylogenetic analyses and nucleotide sequence comparison data demonstrated that WEEV also acquired the genes for non-structural proteins from the EEEV-like ancestor (Weaver et al, 1993).…”

Section: Introductionmentioning

confidence: 90%

Virulence variation among isolates of western equine encephalitis virus in an outbred mouse model

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Bosio

Welte

et al. 2009

Journal of General Virology

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Little is known about viral determinants of virulence associated with western equine encephalitis virus (WEEV). Here, we have analysed six North American WEEV isolates in an outbred CD1 mouse model. Full genome sequence analyses showed ¡2.7 % divergence among the six WEEV isolates. However, the percentage mortality and mean time to death (MTD) varied significantly when mice received subcutaneous injections of 10 3 p.f.u. of each virus. Two WEEV strains, McMillan (McM) and Imperial 181 (IMP), were the most divergent of the six in genome sequence; McM caused 100 % mortality by 5 days post-infection, whereas IMP caused no mortality. McM had significantly higher titres in the brain than IMP. Similar differences in virulence were observed when McM and IMP were administered by aerosol, intranasal or intravenous routes. McM was 100 % lethal with an MTD of 1.9 days when 10 3 p.f.u. of each virus was administered by intracerebral inoculation; in contrast, IMP caused no mortality. The presence of IMP in the brains after infection by different routes and the lack of observed mortality confirmed that IMP is neuroinvasive but not neurovirulent. Based on morbidity, mortality, MTD, severity of brain lesions, virus distribution patterns, routes of infection and differences in infection of cultured cells, McM and IMP were identified as high-and low-virulence isolates, respectively.

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Section: Introductionmentioning

confidence: 90%

Virulence variation among isolates of western equine encephalitis virus in an outbred mouse model

Logue

Bosio

Welte

et al. 2009

Journal of General Virology

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“…This may be explained by the fact that CHIKV shares 85% of homology with the structural polyprotein of ONNV but only 44 to 62% with that of other alphaviruses (1,38). Indeed, ONNV was initially thought to belong to the CHIKV group (39).…”

Section: The Journal Of Immunologymentioning

confidence: 99%

Chikungunya Virus Envelope-Specific Human Monoclonal Antibodies with Broad Neutralization Potency

Warter

Lee

Thiagarajan

et al. 2011

The Journal of Immunology

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Chikungunya virus (CHIKV) is an alphavirus responsible for numerous epidemics in Africa and Asia. Infection by CHIKV is often characterized by long-lasting, incapacitating arthritis, and some fatal cases have been described among elderly and newborns. Currently, there is no available vaccine or specific treatment against CHIKV. Blood B cells from a donor with history of CHIKV infection were activated, immortalized, amplified, and cloned. Two human mAbs against CHIKV, 5F10 and 8B10, were identified, sequenced, and expressed in recombinant form for characterization. In a plaque reduction neutralization test, 5F10 and 8B10 show mean IC50 of 72 and 46 ng/ml, respectively. Moreover, both mAbs lead to a strong decrease in extracellular spreading of infectious viral particles from infected to uninfected cells. Importantly, the mAbs neutralize different CHIKV isolates from Singapore, Africa, and Indonesia, as well as O’nyong-nyong virus, but do not recognize other alphaviruses tested. Both mAbs are specific for the CHIKV envelope: 5F10 binds to the E2 glycoprotein ectodomain and 8B10 to E1 and/or E2. In conclusion, these two unique human mAbs strongly, broadly, and specifically neutralize CHIKV infection in vitro and might become possible therapeutic tools against CHIKV infection, especially in individuals at risk for severe disease. Importantly, these mAbs will also represent precious tools for future studies on host–pathogen interactions and the rational design of vaccines against CHIKV.

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“…Genomic viral RNA was extracted directly from 0.2 ml of virus seed as previously described. 39 The precipitated RNA was dissolved in 50 40 eastern equine encephalitis, 41,42 western equine encephalitis, 43 Ross River, 44 Aura, 45 Semliki Forest, [46][47][48] and O'nyong-nyong 49 viruses. The cG14T.KEP amplimer ( Table 2) was designed to anneal to the 3Ј-terminal C residue and the immediately following 14 A residues of the poly(A) tail of the alphavirus genome.…”

Section: Virusesmentioning

confidence: 99%

Nucleotide sequences of the 26S mRNAs of the viruses defining the Venezuelan equine encephalitis antigenic complex.

Kinney

Pfeffer²,

Tsuchiya³

et al. 1998

The American Journal of Tropical Medicine and Hygiene

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Abstract. Genetic relationships among viruses defining the Venezuelan equine encephalitis (VEE) virus antigenic complex were determined by analyzing the 3Ј-terminal 561 nucleotides of the nonstructural protein 4 gene and the entire 26S RNA region of the genome. New sequence information is reported for VEE 78V-3531 (VEE subtypevariety IF), Mucambo (IIIA), Tonate (IIIB), 71D-1252 (IIIC), Pixuna (IV), Cabassou (V), and AG80-663 (VI) viruses. The results reported here and by previous investigators largely support the current classification scheme of these viruses, while clearly identifying Everglades (II) as a subtype I virus. A genetic relationship between 78V-3531 (IF) and AG80-663 (VI) viruses contradicted previous serologic results. Mutations near the amino terminus of the E2 envelope proteins of Pixuna and AG80-663 viruses probably account for the previously reported low reactivity of the protective monoclonal antibody 1A2B-10 with these two viruses. Variations in the distribution of potential glycosylation sites in the E2 glycoprotein are discussed.Venezuelan equine encephalitis (VEE) viruses are mosquito-borne members of the genus Alphavirus, family Togaviridae. The viral genome is a positive-sense, 5Ј-capped, 3Ј-polyadenylated RNA genome of about 11.5 kilobases. Four nonstructural proteins are encoded in the 5Ј two-thirds of the genome. The structural proteins are processed from a precursor polyprotein (NH 2 -capsid-E3-E2-6K-E1-COOH) that is translated from an intracellular, subgenomic 26S mRNA molecule, which is itself transcribed from the 3Ј onethird portion of the genomic mRNA. The mature virus is composed of an icosahedral nucleocapsid that is surrounded by a lipid envelope containing the viral E1 and E2 glycoproteins.

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Complete sequence of the genomic RNA of O'Nyong-Nyong virus and its use in the construction of alphavirus phylogenetic trees

Cited by 114 publications

References 25 publications

Virulence variation among isolates of western equine encephalitis virus in an outbred mouse model

Virulence variation among isolates of western equine encephalitis virus in an outbred mouse model

Chikungunya Virus Envelope-Specific Human Monoclonal Antibodies with Broad Neutralization Potency

Nucleotide sequences of the 26S mRNAs of the viruses defining the Venezuelan equine encephalitis antigenic complex.

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