September 28, 2020
In a study published in Autophagy, researchers at the University of Maryland (UMD) shed new light on how Zika virus hijacks our own cellular machinery to break down a protein that is essential for neurological development and cellular communication, getting it to “eat itself”. By triggering this process known as autophagy, Zika virus is able to degrade an important protein, a process that may contribute to the development of neurological or brain deficiencies and congenital birth defects in the newborns of infected pregnant women. By understanding the underlying mechanisms of how this process takes place, researchers are coming closer to developing therapeutic interventions to prevent congenital birth defects such as microcephaly caused by Zika virus infection in pregnant mothers.
“The Zika virus is able to disrupt our cellular mechanisms to create a conducive environment to replicate,” explains Yanjin Zhang, associate professor in Veterinary Medicine at UMD. “It upregulates some proteins and downregulates others that have antiviral roles, manipulating and interfering with cells to its own advantage. In this case, it looks like the KPNA2 protein may have some antiviral effects, so the virus uses the natural cellular self-destruction process called autophagy, or self-eating, to get rid of KPNA2.”