Zika Research Projects List: The crystal structure of Zika virus helicase: basis for antiviral drug design

Abstract

The genus of Flavivirus contains important human pathogens, including dengue (DENV), yellow fever (YFV), West Nile (WNV), Japanese encephalitis (JEV), and tick-borne encephalitis (TBEV) viruses, which cause a number of serious human diseases throughout the world (Pierson TC, 2013). Zika virus (ZIKV) is also an arthropod-borne flavivirus, which was initially isolated in 1947 from a febrile sentinel rhesus monkey in the Zika forest in Entebbe, Uganda. ZIKV is transmitted by multiple Aedes mosquitoes (Lazear and Diamond, 2016). Historically, ZIKV infection typically caused a mild and self-limiting illness in human beings, accompanied by fever, headache, arthralgia, myalgia, and maculopapular rash (Ioos et al., 2014). ZIKV caught global attention in April 2007, when it caused a large epidemic of Asian genotype ZIKV in Yap Island and Guam, Micronesia. From 2013 to 2014, the Asian genotype was found responsible for the epidemics among several Pacific Islands, including French Polynesia, New Caledonia, Cook Islands, Tahiti, and Easter Island (Lazear and Diamond, 2016). In 2015, a rampant outbreak of ZIKV infection struck Brazil and other regions of the Americas, causing an estimated 1.3 million cases (Hennessey et al., 2016; Mlakar et al., 2016). Thereafter, ZIKV was found in fetal brain tissue, presumably accounting for the sharp increase of congenital microcephaly in the epidemic areas (Brasil et al., 2016; Mlakar et al., 2016; Rodrigues, 2016). Recent studies have demonstrated the significant cellular death of neural stem cells once infected with ZIKV, which provides direct evidence for the inhibitory role of ZIKV on fetal brain development (Tang et al., 2016). However, as there are currently no effective vaccines or therapies available to contain ZIKV infection, ZIKV remains a significant challenge to the public health of the Western Hemisphere as well as the whole world (Lazear and Diamond, 2016).