Malaria Drug Shown to Protect Against Zika, NIH Says

July 10, 2017

The National Institutes of Health says a new study showed that hydroxychloroquine reduced the transmission of Zika in pregnant mice.

On July 10, 2017, the National Institutes of Health (NIH) announced that a study found that hydroxychloroquine, an FDA-approved drug to treat malaria and autoimmune diseases in pregnant women, reduced transmission of Zika virus in pregnant mice to their fetuses.

According to NIH, hydroxychloroquine inhibits autophagy, the process cells use to remove toxins and recycle damaged components to generate energy. According to the NIH researchers, the Zika virus may manipulate this process in the placenta to infect the developing fetus. Therefore, the researchers believed that autophagy-inhibiting drugs may help lower the transmission of the virus.

“Zika virus infection during pregnancy can lead to a devastating array of birth defects, including microcephaly, abnormal reflexes, epilepsy, and problems with vision, hearing and digestion,” said Catherine Y. Spong, M.D., deputy director of NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), in a press release. “This study suggests that treating Zika-infected pregnancies with autophagy-inhibiting drugs may lower the risk of these abnormalities, but more research is needed to confirm these findings.”

In the study, the researchers led by Indira U. Mysorekar, PhD, at the Washington University School of Medicine in St. Louis, showed that Zika activates autophagy in lab cultures of human placental cells and in the placentas of mouse models of Zika transmission. They found that Zika-infected pregnant mice that lacked an essential autophagy gene called Atg16l1 had less detectable virus and less fetal damage compared to Zika-infected mice to had the Atg16l1 gene.

The researchers then gave hydroxychloroquine to Zika-infected pregnant mice. The mice treated with hydroxychloroquine “had lower levels of detectable virus in their placentas and less placental damage compared to untreated mice.”

“Our findings indicate that pharmacological inhibition of autophagy warrants evaluation in preclinical studies and eventually in human trials to further define its effects on Zika congenital disease,” added Dr. Mysorekar.

The study was published online in the Journal of Experimental Medicine and was partially funded by NIH. The study received additional funding from the Burroughs Wellcome Fund, the March of Dimes and NIH’s National Institute of Allergy and Infectious Diseases.

Source: NIH