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Review
. 2004 Oct;2(10):789-801.
doi: 10.1038/nrmicro1006.

Transmission cycles, host range, evolution and emergence of arboviral disease

Affiliations
Review

Transmission cycles, host range, evolution and emergence of arboviral disease

Scott C Weaver et al. Nat Rev Microbiol. 2004 Oct.

Abstract

Many pandemics have been attributed to the ability of some RNA viruses to change their host range to include humans. Here, we review the mechanisms of disease emergence that are related to the host-range specificity of selected mosquito-borne alphaviruses and flaviviruses. We discuss viruses of medical importance, including Venezuelan equine and Japanese encephalitis viruses, dengue viruses and West Nile viruses.

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Conflict of interest statement

The authors declare no competing financial interests.

Figures

Figure 1
Figure 1. Locations of Venezuelan equine encephalitis virus outbreaks in the Americas.
Map showing the locations of all major Venezuelan equine encephalitis (VEE) outbreaks in the Americas (regions shaded purple and labelled with text). The date of the outbreak (year) and the VEE virus (VEEV) subtypes that caused the outbreak are shown. Symbols represent locations from which enzootic VEEV-complex viruses have been isolated, with enzootic subtypes indicated in parentheses.
Figure 2
Figure 2. Venezuelan equine encephalitis emergence — a phylogenetic tree.
Phylogenetic tree showing the evolutionary history of Venezuelan equine encephalitis virus (VEEV) emergence derived from gene sequences encoding the PE2 envelope glycoprotein precursor (1,677 nucleotides) using neighbour-joining analysis. VEEV strains are denoted by subtype, followed by country and strain designation. Epizootic strains isolated during equine epizootics are shown in red (VEEV subtypes IAB, IC and IE). The six main enzootic lineages of VEEV are labelled in black. The ancestral phenotypes (enzootic or epizootic) were reconstructed by minimizing phenotypic changes in the branches (treating the phenotype as a character with the most parsimonious reconstruction). Numbers indicate bootstrap values — a measure of how probable the groupings represent descendants of a common ancestor. Reproduced with permission from Ref. © (2002) American Society for Microbiology.
Figure 3
Figure 3. Phylogenetic trees of Japanese encephalitis virus.
a | Neighbour-joining phylogeny of complete Japanese encephalitis virus (JEV) genomes, with a representative strain from other viruses in the JEV serogroup outgrouped using Dengue-2 strain New Guinea C (Den2 NGC). Indonesian isolates are shown in red. b | Neighbour-joining phylogeny of envelope genes, outgrouped using Murray Valley encephalitis (MVE) strain 1-51. Indonesian isolates are shown in red. The tree was constructed using more than 200 isolates from all geographical areas, but for clarity, only a representative isolate of each genotype from each geographical area is shown. Genotypes (I—V) are shown on the right of each tree. Bootstrap values, given as a percentage of 1,000 replicates, are indicated. KUN, Kunjin; SLE, St Louis encephalitis; WN, West Nile. Reproduced with permission from Ref. © (2003) American Society for Microbiology.
Figure 4
Figure 4. Evolutionary history of dengue virus emergence.
Phylogenetic tree derived from envelope-protein gene sequences (1,512 nucleotides) using neighbour-joining analysis. Endemic strains isolated from humans or peridomestic vectors are shown in purple and sylvatic strains isolated from non-human primates or arboreal mosquitoes are shown in green. Because the phenotypic change from sylvatic to endemic transmission could have occurred at any point along the indicated branches (shown by pink arrow boxes), time estimates for dengue emergence are represented by maximal values plus one standard deviation (derived from synonymous substitution rate estimates). DENV, dengue virus. Reproduced with permission from Ref. © (2000) American Society for Microbiology.

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