From Science Daily
January 5, 2018
When exposed to Zika virus before birth, mouse fetuses with the protein commit cell suicide, while fetuses without it continued to develop. The result, published January 5 in Science Immunology, suggests that the protein, a receptor involved in immune cell signaling, plays a role in spontaneous abortions and other human pregnancy complications.
The work could have implications for pregnant women infected with Zika or women with autoimmune disorders who are trying to have a baby, says study author Akiko Iwasaki, a Howard Hughes Medical Institute (HHMI) investigator and immunologist at Yale University.
“Pregnancy is a huge investment for a mother,” she says. “Our work shows how this signaling pathway works to terminate pregnancies that are not going to be viable early on.”
Zika virus is carried and transmitted by the Aedes aegypti mosquito and can also be spread during sex. Scientists have linked infections during pregnancy to stillbirths and birth defects such as microcephaly, where a baby’s head is abnormally small. Iwasaki and other researchers have been studying how signaling proteins called interferons defend the body against the virus.
“Interferons are one of the most potent antiviral factors the body generates,” Iwasaki says. When the body detects a virus, cells release interferons, which mount a rapid immune defense. Past studies have shown that adult mice lacking the receptor that binds two types of interferons, interferon-α and interferon-β, are highly susceptible to Zika. But the receptor’s effect on infected fetuses was unknown.