In the event of a Zika infection, the placenta is unable to shield a fetus from the disease, a new study has found. Instead of nourishing the growing embyro, it seems to give way for the infection’s growth and journey into the developing brain of the fetus.
Emory University researchers have discovered that the virus can infect and proliferate in immune cells from the placenta without killing them, which could explain how it passes through the placenta to wreak havoc on the developing brain cells of a fetus and cause terrible birth defects.
"Our results substantiate the limited evidence from pathology case reports," said senior study author and pediatrics professor Dr. Mehul Suthar, emphasizing that little was known about the exact mechanism through which the virus replicates in the placenta.
Related viruses such as dengue, West Nile, and yellow fever rarely transmit from the mother to the fetus, and this is believed to be due to the placenta’s protective role. Zika, Suthar said, has a unique capacity to infect placenta cells and cross its barrier.
Using cells donated by healthy women who had full-term Cesarean births, the researchers saw surprising results: the Zika virus did not kill Hofbauer cells, which are protective cells produced by growing fetuses. Instead, it continued reproducing.
Unlike other immune cells in the placenta, Hofbauer cells are derived from the fetus and not from the mother. They are believed more tolerant and less sensitive to inflammatory reactions than other immune cells.
The researchers, however, detected signs of inflammatory and antiviral response in infected Hofbauer cells, raising the questions of which receptors allow the virus to enter these cells, and whether or not they alter their immune status during the varying phases of pregnancy.
The results help explain why the first and early second trimesters of pregnancy pose the highest risk for Zika infection — the placenta is not developed enough at those phases to ward off an infection. Resistance to Zika, though, varies from one donor to another, partly explaining why not every pregnant woman infected by Zika has a baby suffering the virus.
"Host genetics and non-viral factors, including nutrition and microbiota, as well as timing may be influencing infectivity," Suthar explained, adding that understanding these factors better could help design effective antiviral treatments and preventive measures.
The strain of the virus used in the study came from Puerto Rico, similar to the one currently circulating in Brazil.
The findings were published May 27 in the journal Cell Host & Microbe.
Three groundbreaking studies also recently showed how the mosquito-borne virus reaches and damages brain cells in pregnant mice's fetuses.
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