Two new studies are providing some additional insight and hope for treating the effects of the Zika virus. One study looked at the immune response to the infection and the other looked at utilizing an existing drug for another mosquito-borne disease as a prospective preventive treatment.
Upon its discovery in 1947, the Zika virus was thought to cause only mild infection. Today, thanks to a presumed mutation in the virus
, infections can cause devastating birth defects, such as microcephaly
, and lead to Guillain-Barré Syndrome (GBS
) in adults. A new study
from Yale University researchers has linked the virus with nerve damage as well.
Through the use of mice models that lacked “a key antiviral response,” investigators, led by immunobiologist Akiko Iwasaki, PhD, found that “infection with Zika virus causes paralysis and death,” according to a press release
on the research. The investigators set out to understand why this occurred, and what they found was that “when the Zika infection spreads from the circulating blood into the brain, immune cells known as CD8 T cells flood the brain.” These immune cells activate Zika-related paralysis, even though they inhibit infection of nerve cells. According to Dr. Iwasaki, “The immune cells that are generated by infection start attacking our own neurons. The damage is not occurring through the virus infection, but rather the immune response to the virus.”
The investigators postulate that these findings can help to understand some of the effects seen from Zika virus infection, such as GBS. In addition, therapy efforts that tackle the immune response may aid in treating the syndrome.
Treatment for the Zika virus itself is being studied by a team in California
. There, investigators looked at how an existing treatment—the antimalaria drug, chloroquine, which is known to be safe to use during pregnancy—could reduce the transmission of the Zika virus from a mother to her unborn fetus.
After providing a humanized dose of chloroquine to pregnant mice through drinking water, the investigators from Sanford Burnham Prebys Medical Discovery Institute and the University of California San Diego School of Medicine, both located in San Diego California, found that chloroquine “markedly reduced the amount of Zika virus in maternal blood and neural progenitor cells in the fetal brain,” according to a press release
When speaking on the ramifications of these results in the press release, co-senior author, Alysson R. Muotri, PhD, professor and director of the Stem Cell Program at UC San Diego stated, “Our research is the first to study Zika infection in a mouse model that transmits the virus in a way similar to humans. Until now, researchers used a mouse strain that is deficient in interferon—a signaling protein that heightens anti-viral defenses. Those mice actually die from Zika infection, making it difficult to study the natural transmission of the virus from father and mother to fetus and to assess the effect of this transmission on the newborns. We believe our mouse model more accurately represents the way Zika virus infects men, women, and babies while in the womb. Although chloroquine didn't completely clear Zika from infected mice, it did reduce the viral load, suggesting it could limit the neurological damage found in newborns infected by the virus.”
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