Zika virus evolution and spread in the Americas

Abstract

Although the recent Zika virus (ZIKV) epidemic in the Americas and its link to birth defects have attracted a great deal of attention1,2, much remains unknown about ZIKV disease epidemiology and ZIKV evolution, in part owing to a lack of genomic data. Here we address this gap in knowledge by using multiple sequencing approaches to generate 110 ZIKV genomes from clinical and mosquito samples from 10 countries and territories, greatly expanding the observed viral genetic diversity from this outbreak. We analysed the timing and patterns of introductions into distinct geographic regions; our phylogenetic evidence suggests rapid expansion of the outbreak in Brazil and multiple introductions of outbreak strains into Puerto Rico, Honduras, Colombia, other Caribbean islands, and the continental United States. We find that ZIKV circulated undetected in multiple regions for many months before the first locally transmitted cases were confirmed, highlighting the importance of surveillance of viral infections. We identify mutations with possible functional implications for ZIKV biology and pathogenesis, as well as those that might be relevant to the effectiveness of diagnostic tests.

Molecular mapping of Zika spread

“…Previously thought of as mild, Zika has revealed a potent capa city to damage developing neurological tissues, with devastating consequences for the children of infected mothers 1 . Three related papers [2][3][4] in this issue provide much-needed insight into when, where and how the current Zika outbreak emerged and spread. This understanding was gained thanks to a mixture of high-tech molecular-biology and evolutionary techniques, and low-tech sample-collection efforts.…”

“…material from low-quality samples 3,10,11 . And it can build on the techniques deployed in the current studies.…”

Consequences of congenital Zika virus infection

“…Humans are incidental dead-end hosts for many of the encephalitic flaviviruses including WNV, JEV, SLEV, POWV and TBEV, which depend on amplification by transmission between non-human hosts and arthropod vectors [29–31]. By contrast, DENV, YFV, and ZIKV can perpetuate transmission between humans and mosquitos [1,31–33]. Many flaviviruses (e.g., SLEV and POWV) cause only small outbreaks in humans, whereas other flaviviruses (e.g., ZIKV, TBEV, YFV, and DENV) have caused larger outbreaks [1,34].…”

Infection via mosquito bite alters Zika virus replication kinetics in rhesus macaques

“…The exact 281 threshold viremia that results in productive mosquito infection remains unknown, but a recent 282 study used artificial membrane feeding to establish a minimum infective dose of 4.2 log 10 283 PFU/ml for susceptibility in mosquitoes 42 . It should be noted that viral loads in macaque plasma 284 resemble those reported in humans in endemic areas 32,[43][44][45]45,46 . Furthermore, the first clinical 285 description of a patient suffering from Zika fever was reported in 1956, and was based on a 286 ZIKV infection experimentally induced in a human volunteer 47 .…”