Abstract
Zika virus (ZIKV) is an emerging mosquito-borne virus that can cause ZIKV congenital syndrome when a pregnant woman is infected. Sexual transmission has also been described for ZIKV, though the relationship between sexual transmission and vertical transmission has not been investigated. Here, viral dissemination to the female reproductive tract and fetuses was assessed in immunodeficient (AG129) female mice that were exposed to ZIKV by subcutaneous (s.c.) inoculation, intravaginal (ivag.) inoculation, or sexual transmission from infected male AG129 mice. Pregnant females had significantly increased ZIKV dissemination to the female reproductive tract compared to non-pregnant females when exposed by s.c. or ivag. inoculation. Sexual transmission resulted in significantly greater morbidity and mortality in females and higher ZIKV titers in the female reproductive tract than s.c. or ivag. inoculation. Ovaries from females infected sexually contained ZIKV RNA within the ovarian follicles. Furthermore, ZIKV titers were significantly higher in fetuses from dams exposed sexually compared to fetuses from dams exposed by s.c. or ivag. inoculation. These results demonstrate that sexual transmission enhances dissemination of ZIKV to the female reproductive tract and developing fetuses in a mouse model.
Highlights
Zika virus (ZIKV) is an emerging mosquito-borne virus that can cause ZIKV congenital syndrome when a pregnant woman is infected
Sexual transmission of ZIKV leads to more rapid disease in female AG129 mice
ZIKV was detected by in situ hybridization (ISH) within the uterine vasculature of both non-pregnant and pregnant females and in association with neutrophilic inflammation in the myometrium of one non-pregnant animal, and within placental sites, including trophoblasts, of pregnant females by ISH and IHC (Fig. 4D,E).These findings suggest the potential for transplacental ZIKV transmission to the fetus, as well infection from the maternal decidua
Summary
Zika virus (ZIKV) is an emerging mosquito-borne virus that can cause ZIKV congenital syndrome when a pregnant woman is infected. Viral dissemination to the female reproductive tract and fetuses was assessed in immunodeficient (AG129) female mice that were exposed to ZIKV by subcutaneous (s.c.) inoculation, intravaginal (ivag.) inoculation, or sexual transmission from infected male AG129 mice. These results demonstrate that sexual transmission enhances dissemination of ZIKV to the female reproductive tract and developing fetuses in a mouse model. Pregnant immunodeficient mouse models of ZIKV have shown in utero transmission following intravaginal inoculation[19], subcutaneous inoculation[20], and sexual transmission[21,22,23] These and other studies of ZIKV infection in pregnant, immunodeficient female mice have demonstrated intrauterine growth restriction, fetal demise, fetal brain infection, and decreased cranial size of infected fetuses[24]. Transplacental infection of the fetus has been implicated by infection of placental trophoblasts in human placentas[25,26,27,28] and pregnant mice[20] and monocytes from human placentas[29], though other studies have shown trophoblasts from
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