Abstract
In humans, Zika virus and viral RNA have been detected in semen up to 2.2 months and 6 months post infection (pi), respectively. Although the contribution of sexual transmission to the spread of ZIKV is too low to sustain an outbreak, it can increase the risk of infection and the epidemic size as well as prolong the duration of an outbreak. In this study, we explored the potential of antivirals to serve as an effective strategy to prevent sexual transmission. Male AG129 mice infected with a ZIKV isolate from Suriname were treated with the nucleoside analog, 7-deaza-2′-C-methyladenosine (7DMA), that was previously shown to be efficacious in reducing ZIKV viremia and delaying ZIKV-induced disease in mice. Following treatment, viral RNA and infectious virus titers were consistently reduced in the male reproductive organs compared to vehicle-treated mice. This reduction of ZIKV loads in the testis was confirmed by the detection of lower levels of ZIKV antigens. Our data illustrate the value of this mouse model to validate the efficacy of new potential ZIKV drugs at the level of the male reproductive system.
Highlights
Zika virus (ZIKV) is a re-emerging, arthropod-borne virus, belonging to the family of Flaviviridae
We previously demonstrated the ability of 7-deaza-2 -C-methyladenosine (7DMA) to delay ZIKV-induced disease in AG129 mice when administered at the time of or two days prior to infection [20]
We evaluated the antiviral efficacy of 7DMA on ZIKV loads in the male reproductive organs
Summary
Zika virus (ZIKV) is a re-emerging, arthropod-borne virus (arbovirus), belonging to the family of Flaviviridae. No further transmission was identified in the Pacific until October 2013, when an outbreak occurred in French Polynesia, followed by the emergence of ZIKV on other Pacific islands [2]. Recent studies showed that ZIKV can be sexually transmitted between humans, with male to female transmission being the most common. The low contribution (~1%) of sexually transmitted ZIKV cases to the overall epidemiology was confirmed in recent reviews [17,18]. These models suggest that, the contribution of sexual transmission is too low to sustain an outbreak, it can increase the risk of infection and epidemic size as well as prolong the duration of an outbreak. We describe the utility of this model to evaluate the use of antiviral molecules as a strategy against sexual transmission of ZIKV by reducing the viral load in male reproductive organs
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