Zika virus: History, emergence, biology, and prospects for control

Abstract

Zika virus (ZIKV), a previously obscure flavivirus closely related to dengue, West Nile, Japanese encephalitis and yellow fever viruses, has emerged explosively since 2007 to cause a series of epidemics in Micronesia, the South Pacific, and most recently the Americas. After its putative evolution in sub-Saharan Africa, ZIKV spread in the distant past to Asia and has probably emerged on multiple occasions into urban transmission cycles involving Aedes (Stegomyia) spp. mosquitoes and human amplification hosts, accompanied by a relatively mild dengue-like illness. The unprecedented numbers of people infected during recent outbreaks in the South Pacific and the Americas may have resulted in enough ZIKV infections to notice relatively rare congenital microcephaly and Guillain-Barré syndromes. Another hypothesis is that phenotypic changes in Asian lineage ZIKV strains led to these disease outcomes. Here, we review potential strategies to control the ongoing outbreak through vector-centric approaches as well as the prospects for the development of vaccines and therapeutics.

Copyright © 2016 Elsevier B.V. All rights reserved.

Figures

Fig. 1

Map showing the known distribution of Zika virus based on serosurveys, virus detection, and laboratory-diagnosed cases. Blue arrows show recent patterns of spread deduced from phylogenetic studies (see Fig. 3). The yellow star shows the location of the Zika forest where the virus was discovered in 1947.

Fig. 2

Sylvatic or enzootic Zika virus transmission cycles in Africa with potential vectors and vertebrate amplification/reservoir hosts and putative patterns of emergence into the urban human-mosquito-human transmission cycle. References for vector implications are found in the text in section 6.

Fig. 3

Phylogenetic tree of the genus Flavivirus showing the position of Zika virus within the group of viruses vectored by Aedes spp. mosquitoes. Selected flavivirus sequences representing a 2,757 nt portion of the polymerase (NS5) gene were aligned manually using the Se-Al application based on amino acid sequence alignments. A Neighbor-Joining tree was built based on this alignment using PAUP* v4.0b package. A maximum likelihood (ML) tree was then inferred using PAUP* based on the best-fit substitution model estimated from Modeltest version 3.06.19. The optimal ML tree was estimated using the appropriate model and a heuristic search with tree-bisection-reconstruction branch swapping and 1000 replicates, estimating variable parameters from the data, where necessary. Bootstrap replicates were calculated for each dataset under the same models mentioned above. The scale shows 20% nucleotide sequence divergence

Fig. 4

Phylogenetic tree of Zika virus strain complete open reading frame sequences inferred using maximum likelihood methods in MEGA6.0, employing the GTI + I model, and either nearest-neighbor interchange (NNI) and subtree pruning and regrafting branch swapping. The phylogenetic robustness of each node was determined using 1,000 bootstrap replicates and NNI branch swapping. Strain names signify abbreviated country/virus/strain/year of collection (SPOV – Spondweni; KEDV – Kedougou virus), and numbers indicate bootstrap values