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Zika virus (ZIKV), the mosquito-borne Flavivirus, became widely known during a pandemic in Brazil in 2015, in which approximately 1.5 million people were infected (WHO, 2016; Marinho et al., 2016; Jang et al., 2015). Since then, ZIKV transmission has been reported in 64 countries around the world (Stauft et al., 2016). The emergence of newborns with microcephaly was first reported during the outbreak in Brazil, in which 4,700 diseased infants were observed (Calvet et al., 2016). Owing to the severity of the symptoms, the WHO declared a state of emergency against Zika virus infection on February 1, 2016, emphasizing the risk of infection to the global population (WHO, 2016).
ZIKV was first isolated from a rhesus monkey in a study of yellow fever in the Zika forest of Uganda in 1947 (Dick et al., 1952). Over the next 20 years, ZIKV was isolated in East and West Africa in the absence of epidemics, and spread from Africa to Southeast Asia (Moore et al., 1975; Fagbami, 1979). In April 2007, the first pandemic was reported in Yap Island of the Federated States of Micronesia in the Western Pacific Ocean, with about 100 infected patients (Duffy et al., 2009). ZIKV was also responsible for an outbreak in French Polynesia in the South Pacific Ocean in 2013, in which approximately 30,000 people were infected (Cao-Lormeau et al., 2014). Since 2014, ZIKV spread across the Pacific Ocean to South America, Central America, and the Caribbean, and finally reached Brazil, resulting in an explosive outbreak (Fauci & Morens, 2016; Rubin et al., 2016).
The complete genome sequence of ZIKV is now available. The genome is divided into three structural genes, C, prM, and E, and seven nonstructural (NS) genes, NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5 (Kuno & chang, 2007). These genes are arranged in the following order in the genome: 5′-capsid (C)-premembrane (prM)-envelope (E)-NS1-NS2A-NS2B-NS3-NS4A-NS4B-NS5-3′ (Zhu et al., 2016). According to our previous study, these 10 genes exhibit differentiation among regions (Jooyeon et al., 2016). A phylogenetic analysis revealed that the genome sequence of ZIKV exhibits regions of conservation and divergence. The capsid, pre-membrane, NS2B, NS3, and NS4A genes tend to be conserved among regions owing to their important roles in the viral life cycle and replication. The envelope, NS1, NS2A, NS4B, and NS5 genes evolve more rapidly to adjust to regional hosts.
ZIKV has two distinct geographical lineages, Asian and African (Enfissi et al., 2016). However, there is not a strong association between geographical lineages and continent-specific viral properties. Even within the Asian lineage, isolates from Southeast Asia and South America have different infection propensities. For example, ZIKV infections in Brazil are characterized by a higher number of babies with microcephaly than infections in Southeast Asia. These observations indicate that sequence variation on each continent must be considered in addition to the differences between Asian and African lineages. In this study, we investigated sequence differences in 10 genes between ZIKV from six continents and examined the relationships between regional features and genetic characteristics.