The journal Science Immunology highlighted Yale research in the journal’s first-ever Facebook Live.
Researchers at the Yale School of Medicine discovered that a protein designed to protect the body from infection by the Zika virus also disrupts fetal development and potentially terminates pregnancies in Zika-infected mothers. The authors of the study postulated that, therefore, immune response may also have an evolutionary purpose to end the pregnancy, so that the mother may pursue a healthier pregnancy in the future. The study was first published on Jan. 5.
Anand Balasubramani, an editor at Science Immunology, introduced the research at the outset of the Facebook Live, noting the previous lack of information on how Zika virus in mothers affects fetal development.
“This study has really changed the landscape for strategies of how to prevent Zika-associated abnormalities in newborns,” he said.
The Facebook Live was held on Thursday at 2 p.m. and featured three of the study’s co-authors, as well as two moderators from the journal. The study authors took turns introducing the study and its results, before a Q&A period featuring queries from both the moderators and Facebook commenters. The Facebook Live, which lasted half an hour, was viewed live by approximately 400 people, and in the days following has garnered upwards of 28,000 views.
“I think that more and more scientists should be doing this kind of outreach,” corresponding author Akiko Iwasaki said. “Science is very important, but we are pretty lousy about communicating our research to the public. Every time there is an opportunity, scientists should step up and do these kinds of interviews.”
The study was released as part of an ongoing project on Zika virus that began in 2015, said Iwasaki, a professor of immunobiology. In earlier work, the same team used a mouse model to identify an antiviral protein, called an interferon, that defends the body from Zika virus. To confirm their results, they used a genetic knockout to prevent the interferon from functioning in some of the mice.
In pregnant mice, they found that knocking out the interferon increased the amount of Zika virus found in mouse fetuses. However, they also found that fetuses without the interferon were more likely to develop and live, despite having a larger concentration of the virus, said Laura Yockey MED ’19 GRD ’19, first author of the study. They used this observation to take their mouse model further, testing the development and survival of fetuses in Zika-infected mothers both with and without the disease. What they found was that the interferon that protects both the mother and fetus from Zika virus also damages the placenta and deters development of the fetus, potentially killing it, Yockey said.
“We found that it was the immune response to the virus, rather than the virus itself that is responsible for the growth restriction and often the death of the fetus,” Yockey said.
There is evidence that this mechanism exists in humans as well, Iwasaki said. Women with unusually high levels of interferons often give birth to children with birth defects, likely due to a similar mechanism, she added.
During the Facebook Live, the authors were cautious in recommending any therapeutic implications of their work. According to Yockey, they have received a multitude of questions about whether a therapy that disables the interferon would increase the chance of a successful pregnancy in Zika patients.
“We know that this interferon is really important for blocking viral infection, so we would not advocate using [interferon blocking] as a therapy during pregnancy,” Yockey said. “Only around 10 percent of Zika-infected women suffer complications with their fetus during pregnancy, and blocking the interferon would increase the risk of more virus reaching the fetus.”
These findings may be more applicable to patients who suffer from autoimmune conditions such as lupus, which are characterized by unusually high interferon levels. In a setting where the interferon does not providing the vital immune defense from a virus such as Zika, there is more potential for the results of the study to have a therapeutic impact, Yockey said.
According to the Centers for Disease Control and Prevention, Zika virus was first discovered in 1947 and is named for the Zika Forest in Uganda where it was first isolated.
Maya Chandra | firstname.lastname@example.org