A mutation in the Zika virus (ZIKV) that might have contributed to its rapid spread in the recent epidemic is identified in Nature this week. The mutation is found in a protein that has previously been shown to influence the acquisition of flaviviruses (the family that includes ZIKV and dengue virus, among others) by mosquitoes.
ZIKV, a mosquito-borne flavivirus that is transmitted to humans by Aedes mosquito species, was obscure until outbreaks in French Polynesia (2013–2014) and South America (2015–2016). In previous work, Gong Cheng and colleagues found that nonstructural protein 1 (NS1) can enhance flavivirus infection in mosquitoes. The protein is secreted into the serum of hosts and can overcome an immune barrier in the mosquito gut.
Now, Gong Cheng, Pei-Yong Shi and colleagues show that this mechanism also promotes the acquisition of ZIKV in its mosquito vector, Aedes aegypti. Moreover, they identify a mutation in NS1 that enhances its secretion and increases mosquito acquisition of the virus. This mutation seemed to appear around 2013, in the virus isolates analysed, and the authors conclude that it might have enhanced the transmission of ZIKV during the recent epidemics.