When the Zika virus is contracted by an expectant mother, the placenta cannot shield the fetus from the disease. Instead of working to nourish the fetus, the placenta gives way for the infection to grow and travel to the developing brain of a fetus.
The researchers say that the Zika virus can infect and multiply in immune cells from the placenta without killing these cells, which might explain how the virus passes on to do serious damage to a fetus’ developing brain cells, thus causing severe birth defects.
Senior study author and pediatrics professor D. Mehul Suthar says, “Our results substantiate the limited evidence from pathology case reports.” Prior to this, there has been little information on the exact process through which the virus proliferates in the placenta.
Related mosquito-borne diseases like dengue, West Nile and yellow fever rarely transfer from the mother to the fetus. This is believed to be the role of the placenta, which acts as a protective barrier. Zika, according to Suthar, has the unique ability to penetrate the placenta and penetrate to the fetus.
The researchers studied cells donated by healthy women who had full-term Cesarean births and were surprised to see that the Zika virus did not kill Hofbauer cells, which are the fetus’ protective cells. Instead, the virus continued reproducing. Unlike other immune cells in the placenta, Hofbauer cells are produced by the fetus and not the mother. They are said to be more tolerant and less sensitive to invasions compared to other immune cells.
The researchers did find signs of inflammatory and antiviral responses in the Hofbauer cells infected by Zika, which begs the questions on which receptors allow the virus to enter these cells, and whether or not they change their immune status during the stages of pregnancy.
These findings help shed light on why the first and second trimesters of pregnancy are at the highest risk for Zika infection, as the placenta is not fully developed during these early phases enough to fight off an infection. Resistance to Zika proved to be different among the donors, which also partially explains why not all pregnant women infected by Zika have babies with birth defects caused by the virus.
“Host genetics and non-viral factors, including nutrition and microbiota, as well as timing may be influencing infectivity,” Suthar says. He adds that understanding these factors will open avenues for more effective anti-Zika treatments and better preventive measures.
The strain of the Zika virus used in the study came from Puerto Rico, which is similar to the one plaguing Brazil. The study was published in the journal Cell Host & Microbe.