Researchers in Brazil reported evidence that the Zika virus can cross the placental barrier and infect the fetus, but added that more research is needed to verify that the virus causes microcephaly, according to a case study published online February 17, 2016 in The Lancet Infectious Diseases.
“Previous studies have identified Zika virus in the saliva, breast milk, and urine of mothers and their newborn babies after having given birth. This study reports details of the Zika virus being identified directly in the amniotic fluid of a woman during her pregnancy, suggesting that the virus could cross the placental barrier and potentially infect the fetus,” said lead author Ana María Bispo de Filippis, PhD, head of the flavivirus laboratory at the Oswaldo Cruz Institute in Rio de Janeiro, Brazil.
Microcephaly has become a public health emergency in Brazil, where the incidence was 20 times higher in 2015 than in previous years—nearly 100 cases per 100,000 livebirths, including 76 infant deaths as of January 2016. Although microcephaly has numerous causes, its dramatic rise has geographically overlapped areas with increased reports of Zika virus infection, the authors noted.
In this case study, Dr. de Filippis and colleagues reported on two pregnant women in northern Brazil who had each presented during the first trimester with symptoms of Zika virus infection, including fever, myalgia, and rash. Ultrasounds taken at approximately 22 weeks of gestation diagnosed microcephaly in each of the fetuses. On the recommendation of Brazilian health authorities, the researchers performed amniocentesis on the patients. Genetic testing revealed Zika virus infection in the amniotic fluids of both women.
This finding demonstrated what the researchers suspected but hadn’t confirmed: that the Zika virus can cross the placental barrier and infect the fetus. The researchers also determined that this virus was genetically related to the strain identified during an outbreak of Zika virus in French Polynesia in 2013.
Although these findings suggest that a “causal relation” might exist between Zika virus infection and fetal microcephaly, this study “cannot determine whether the Zika virus identified in these two cases was the cause of microcephaly in the babies. Until we understand the biological mechanism linking Zika virus to microcephaly, we cannot be certain that one causes the other, and further research is urgently needed,” Dr. de Filippis said.
“The next step will be to do case-control studies to estimate the potential risk of microcephaly after Zika virus infection during pregnancy, other fetal or neonatal complications, and long-term outcomes for infected symptomatic and asymptomatic neonates,” wrote Didier Musso, MD, of the Unit of Emerging Infectious Diseases at Institut Louis Malarde in Tahiti, French Polynesia, and David Baud, MD, PhD, of the Institute of Microbiology at the University of Lausanne, in Lausanne, Switzerland, in a related editorial in The Lancet Infectious Diseases.