Preface Host restriction factors are potent, widely expressed, intracellular blocks to viral replication that are an important component of the innate immune response to viral infection. However, viruses have evolved mechanisms of antagonizing restriction factors. Through evolutionary pressure for both host survival and virus replication, an evolutionary “arms race” has developed that drives continuous rounds of selection for beneficial mutations in restriction factor genes and their viral antagonists. Because viruses can evolve faster than their hosts, the modern-day vertebrate innate immune system is optimized to defend against ancient viruses, rather than current viral threats. Thus, the evolutionary history of restriction factors might, in part, explain why humans are susceptible or resistant to the viruses present in the modern world.

SUMMARYCirculation of Zika virus (ZIKV) was first identified in the Western hemisphere in late 2014. Primarily transmitted through mosquito bite, ZIKV can also be transmitted through sex and from mother to fetus, and maternal ZIKV infection has been associated with fetal malformations. We assessed immunodeficient AG129 mice for their capacity to shed ZIKV in semen and to infect female mice via sexual transmission. Infectious virus was detected in semen between 7 and 21 days post-inoculation, and ZIKV RNA was detected in semen through 58 days post-inoculation. During mating, 73% of infected males transmitted ZIKV to uninfected females, and 50% of females became infected, with evidence of fetal infection in resulting pregnancies. Semen from vasectomized mice contained significantly lower levels of infectious virus, though sexual transmission still occurred. This model provides a platform for studying the kinetics of ZIKV sexual transmission and prolonged RNA shedding also observed in human semen.

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