The study also highlights that NS4A from other related viruses, including dengue and yellow fever, similarly interacts with ANKLE2, suggesting a common strategy among these viruses.

Zika strategically hides in pockets formed by ANKLE2, making it harder for the immune system to combat the virus.

Research led by Adam Fishburn indicates that knocking out the ANKLE2 gene in human cells significantly reduces Zika virus replication, underscoring its importance in the virus's lifecycle.

Zika virus's unique ability to cross the placenta is a key factor in its association with microcephaly, a serious birth defect characterized by abnormal brain development.

Viruses like Zika have limited genetic material and rely on host cell proteins such as ANKLE2 to reproduce, as explored by Shah's lab.

Microcephaly, linked to Zika, results in smaller-than-expected head size due to abnormal brain development, posing significant risks during pregnancy.

Priya Shah, an associate professor at the University of California, Davis, emphasized the unfortunate timing of Zika's presence during fetal development.

The interaction between Zika's NS4A protein and ANKLE2 not only boosts the virus's replication efficiency but also aids in evading the immune system's detection.

A recent study published in mBio reveals that the Zika virus exploits a host protein called ANKLE2, which is crucial for brain development, to enhance its reproduction.

Collaboration with researchers from the University of Nevada, Reno, indicates that Zika also utilizes ANKLE2 in mosquito cells, highlighting its significance in both human and insect hosts.

The research received support from the National Institutes of Health and the W. M. Keck Foundation, with contributions from various authors affiliated with multiple institutions.

In Zika-infected cells, ANKLE2 forms clusters around the endoplasmic reticulum, creating pockets that function as virus factories, thereby improving replication.