Localization of four antigenic sites involved in Venezuelan equine encephalomyelitis virus protection

Agapov, Eugene; Разумов, И. А.; Frolov, Ilya; Kolykhalov, Alexander A.; Нетесов, С. В.; Loktev, V. B.

doi:10.1007/bf01309462

Cited by 23 publications

(20 citation statements)

References 15 publications

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“…This E2 region has been shown to be a major neutralization domain for VEE and Sindbis viruses. [30][31][32] The 1942 and 1946 Peruvian isolates shared four amino acid differences with respect to the remaining IAB strains in the E2 region known to include hemagglutination activity: 33 Val versus Ala at E2-147, Thr versus Ile at E2-187, Val versus Ala (or aspartic acid for TC-83) at E2-192, and Ile versus Met at E2-408. Although all of the viruses we sequenced have been antigenically classified as subtype IAB, amino acid differences in the neutralization domain, particularly nonconserved substitutions, might result in some variability in cross-reactivities in neutralization tests.…”

Section: Resultsmentioning

confidence: 99%

Genetic evidence for the origins of Venezuelan equine encephalitis virus subtype IAB outbreaks.

Weaver

Pfeffer

Marriott

et al. 1999

The American Journal of Tropical Medicine and Hygiene

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Abstract. Epizootics of Venezuelan equine encephalitis (VEE) involving subtype IAB viruses occurred sporadically in South, Central and North America from 1938 to 1973. Incompletely inactivated vaccines have long been suspected as a source of the later epizootics. We tested this hypothesis by sequencing the PE2 glycoprotein precursor (1,677 nucleotides) or 26S/nonstructural protein 4 (nsP4) genome regions (4,490 nucleotides) for isolates representing most major outbreaks. Two distinct IAB genotypes were identified: 1) 1940s Peruvian strains and 2) 1938-1973 isolates from South, Central, and North America. Nucleotide sequences of these two genotypes differed by 1.1%, while the latter group showed only 0.6% sequence diversity. Early VEE virus IAB strains that were used for inactivated vaccine preparation had sequences identical to those predicted by phylogenetic analyses to be ancestors of the 1960s-1970s outbreaks. These data support the hypothesis of a vaccine origin for many VEE outbreaks. However, continuous, cryptic circulation of IAB viruses cannot be ruled out as a source of epizootic emergence.

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Section: Resultsmentioning

confidence: 99%

Genetic evidence for the origins of Venezuelan equine encephalitis virus subtype IAB outbreaks.

Weaver

Pfeffer

Marriott

et al. 1999

The American Journal of Tropical Medicine and Hygiene

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“…Selection of N escape variants with MAbs identified a major N domain between E2 residues 182-207 in VEE virus 58,59 and 170-220 in Sindbis virus. 1,[60][61][62] The sequence variation observed in this E2 N domain of VEE virus would be expected for a domain that is subject to immune selection pressures.…”

Section: Discussionmentioning

confidence: 99%

“…8,9 The E2 region containing the most amino acid sequence variation occurred between amino acid positions 178-224. This E2 region has been shown to be a major N domain for VEE 58,59 and Sindbis 1,60-62 viruses. The E2-204 Gly residue was substituted with Ser in 78V-3531 and AG80-663 viruses; this position was deleted in MUC, TON, 71D-1252, PIX, and CAB viruses (Figure 2).…”

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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“…A 1-kb portion of the E2 gene was amplified from RNA isolated from plaques using primers forward 5Ј-GAAGCGACAGACGGGACG-3Ј and reverse 5Ј-GCCTCTTGGTATGTGGCCGC-3Ј. This genome region was selected as it contains described alphavirus neutralization escape epitopes (2,53). Plaque clone isolations, RNA extractions, and sequencing were performed as described above.…”

Section: Cells and Virusesmentioning

confidence: 99%

“…Aedes albopictus (C6/36) mosquito cells were maintained in L-15 medium with 10% NCS, 1% P/S, 1% nonessential amino acids, and 1% tryptose phosphate broth at 28°C without CO 2 .…”

Section: Cells and Virusesmentioning

confidence: 99%

Host Alternation of Chikungunya Virus Increases Fitness while Restricting Population Diversity and Adaptability to Novel Selective Pressures

Coffey

Vignuzzi

2011

J Virol

160

172

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The mechanisms by which RNA arboviruses, including chikungunya virus (CHIKV), evolve and maintain the ability to infect vertebrate and invertebrate hosts are poorly understood. To understand how host specificity shapes arbovirus populations, we studied CHIKV populations passaged alternately between invertebrate and vertebrate cells (invertebrate 7 vertebrate) to simulate natural alternation and contrasted the results with those for populations that were artificially released from cycling by passage in single cell types. These CHIKV populations were characterized by measuring genetic diversity, changes in fitness, and adaptability to novel selective pressures. The greatest fitness increases were observed in alternately passaged CHIKV, without drastic changes in population diversity. The greatest increases in genetic diversity were observed after serial passage and correlated with greater adaptability. These results suggest an evolutionary trade-off between maintaining fitness for invertebrate 7 vertebrate cell cycling, where maximum adaptability is possible only via enhanced population diversity and extensive exploration of sequence space.Emergence of pathogenic RNA viruses is associated with their genomic variability and environmental changes that lead to novel host contacts. Despite these emergence events, the evolutionary processes that mediate arbovirus host range changes are poorly understood, partly since arbovirus evolution is understudied. Arboviruses are transmitted horizontally between arthropod vectors and vertebrate reservoir hosts. They replicate rapidly and achieve large population sizes. Polymerases of RNA viruses lack proofreading to repair errors, leading to one substitution per ϳ10 Ϫ4 nucleotides (nt) copied (11, 36), corresponding to one error per 10-kb genome. This polymerase infidelity leads to diversification that produces closely related but nonidentical RNAs that together form a spectrum of mutants. Although arbovirus mutant spectra have been observed in nature (1,8,20,55,57), the diversity and divergence within the spectrum are not well described, and the phenotypic roles of minority RNAs are unknown. Understanding the mutation distribution in a heterogeneous arbovirus population is important, given that any variant can be favored by selection and ultimately affect fitness (12, 13). However, the relationships between fitness and RNA virus population diversity are poorly understood.Studies with other RNA viruses, including human immunodeficiency virus (HIV) (3, 58, 60), hepatitis C virus (14,15,25), and poliovirus (30, 52), indicate that intrahost population diversity is important for virus evolution, fitness, and pathogenesis. Unlike these vertebrate-only RNA viruses, arboviruses obligately cycle between vertebrates and arthropods, a process that imposes additional selective constraints on evolution and adaptation. Sequence comparisons of RNA arbovirus isolates show that they are relatively stable (18,19), and genetic studies reveal that evolution is dominated by purifying selection (20)(...

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Localization of four antigenic sites involved in Venezuelan equine encephalomyelitis virus protection

Cited by 23 publications

References 15 publications

Genetic evidence for the origins of Venezuelan equine encephalitis virus subtype IAB outbreaks.

Genetic evidence for the origins of Venezuelan equine encephalitis virus subtype IAB outbreaks.

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

Host Alternation of Chikungunya Virus Increases Fitness while Restricting Population Diversity and Adaptability to Novel Selective Pressures

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