A new study suggests that sexual transmission of Zika virus may create a higher risk for fetal disease than transmission via mosquito.
A new study led by researchers from the University of California, Davis, suggests that vaginal transmission of Zika virus may put fetuses at higher risk of infection compared with mosquito transmission of the disease.
Since the Zika virus outbreak began in Brazil in 2015 and spread to North America, public health officials have been tracking the disease and its link to congenital microcephaly and other neonatal neurological disorders. Zika transmission can occur through the bite of an infected Aedes aegypti or Aedes albopictus mosquito, from an infected individual to their sexual partner, through blood transfusion, through exposure in a health care setting, and from an infected mother to her fetus during pregnancy. Because of the risk of fetal brain defects from Zika, the Centers for Disease Control and Prevention (CDC) began a surveillance program tracking laboratory-confirmed cases of Zika in pregnant woman in the United States. As of August 22, 2017, the CDC has found laboratory evidence of possible Zika infection in 2,155 pregnant women in the United States and the District of Columbia, including 95 liveborn infants with birth defects and 8 pregnancy losses with birth defects.
Despite what the health community now knows about how Zika spreads, researchers have much work to do to understand Zika and its effects during pregnancy. In a recent study published in PLOS Pathogens, researchers studied the effects of vaginal inoculation of Zika in 6 rhesus monkeys to better understand the role of sexual transmission of the virus and compare it with previous findings on subcutaneous inoculation. The researchers noted that after subcutaneous inoculation, meant to replicate exposure through a mosquito bite, Zika is quickly detected in blood plasma, less so in urine and saliva, and only rarely in the reproductive tract. In this study, they found that it took 1 to 8 vaginal inoculations to establish a Zika infection in the monkeys, and the virus replicated preferentially in the female reproductive tract following vaginal transmission. In addition, two monkeys that were resistant to infection after 8 inoculations became infected after being treated with the progestin contraceptive Depo-Provera, suggesting that the drug enhances susceptibility to the virus.
Perhaps the most striking finding in the study was that the kinetics of virus replication and dissemination in rhesus monkeys after intravaginal Zika virus inoculation are markedly different than they are after subcutaneous inoculation, authors noted.
"The high levels of Zika virus replication in the female reproductive tract after vaginal inoculation of rhesus macaques was unexpected because virus shedding in genital secretions is difficult to detect after subcutaneous inoculation," noted the authors in a recent press release. "This finding suggests that fetuses may be especially at risk for virus infection, and associated complications, when women acquire Zika virus through sex."
As there is no vaccine for Zika, pregnant women are urged to take measures to prevent exposure and infection. Zika virus RNA has been detected in human semen for up to 6 months following infection, prompting the CDC to issue recommendations that along with protecting themselves from mosquito bites, pregnant women either abstain from sex or use condoms during pregnancy to avoid becoming exposed through their partners.