BACKGROUND
Zika virus (
ZIKV) was recognised as a zoonotic pathogen in
Africa and
southeastern Asia.
Human infections were infrequently reported until 2007, when the first known
epidemic occurred in
Micronesia. After 2013, the
Asian lineage of
ZIKV spread along the
Pacific Islands and
Americas, causing severe
outbreaks with millions of
human infections. The recent
human infections of
ZIKV were also associated with severe
complications, such as an increase in cases of
Guillain-Barre syndrome and the emergence of
congenital Zika syndrome. OBJECTIVES To better understand the recent and rapid expansion of
ZIKV, as well as the presentation of novel
complications, we compared the genetic differences between the African sylvatic lineage and the
Asian epidemic lineage that caused the recent massive
outbreaks. FINDINGS The
epidemic lineages have significant
codon adaptation in NS1
gene to translate these
proteins in
human and
Aedes aegypti mosquito cells compared to the African zoonotic lineage. Accordingly, a Brazilian
epidemic isolate (ZBR) produced more NS1
protein than the MR766 African lineage (ZAF) did, as indicated by proteomic data from
infections of
neuron progenitor cells-derived neurospheres. Although ZBR replicated more efficiently in these
cells, the differences observed in the stoichiometry of
ZIKV proteins were not exclusively explained by the differences in
viral replication between the lineages. MAIN CONCLUSIONS Our findings suggest that natural, silent translational selection in the second half of 20th century could have improved the fitness of
Asian ZIKV lineage in
human and
mosquito cells.