Abstract
Zika virus (ZIKV) is primarily transmitted by Aedes mosquitoes in the subgenus Stegomyia but can also be transmitted sexually and vertically in humans. STAT1 is an important downstream factor that mediates type I and II interferon signaling. In the current study, we showed that mice with STAT1 knockout (Stat1-/-) were highly susceptible to ZIKV infection. As low as 5 plaque-forming units of ZIKV could cause viremia and death in Stat1-/- mice. ZIKV replication was initially detected in the spleen but subsequently spread to the brain with concomitant reduction of the virus in the spleen in the infected mice. Furthermore, ZIKV could be transmitted from mosquitoes to Stat1-/- mice back to mosquitoes and then to naïve Stat1-/- mice. The 50% mosquito infectious dose of viremic Stat1-/- mouse blood was close to 810 focus-forming units (ffu)/ml. Our further studies indicated that the activation of macrophages and conventional dendritic cells were likely critical for the resolution of ZIKV infection. The newly developed mouse and mosquito transmission models for ZIKV infection will be useful for the evaluation of antiviral drugs targeting the virus, vector, and host.
Highlights
Zika virus (ZIKV) is an enveloped, positive sense RNA virus belonging to the Flaviviridae family and is primarily transmitted to humans via the bite of an Aedes aegypti mosquito [1, 2]
ZIKV infection causes damage in many tissues including the brain in adults and newborns, making ZIKV infection an important health issue globally
We demonstrated that ZIKV could be delivered to mice by mosquito bites and transmitted back to Stat1-/- mice
Summary
Zika virus (ZIKV) is an enveloped, positive sense RNA virus belonging to the Flaviviridae family and is primarily transmitted to humans via the bite of an Aedes aegypti mosquito [1, 2]. ZIKV infections cause self-limiting fever, headache, myalgia, and conjunctivitis [1]. A recent large ZIKV outbreak in Brazil in 2015–2016 was linked to an increased incidence of microcephaly and congenital malformations in children born in the epidemic area as a result of ZIKV crossing the placenta of infected mothers [3,4,5,6]. ZIKV infection was linked to GuillainBarresyndrome in adults [7, 8]. After an acute infection phase, ZIKV can establish a persistent infection in the male reproductive tract that can be sexually transmitted [9, 10]. These varied transmission routes and different clinical presentations make ZIKV a serious public health threat
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