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Updated: Jun 2, 2025

Establishing Mouse Models for Zika Virus-induced Neurological Disorders Using Intracerebral Injection Strategies: Embryonic, Neonatal, and Adult

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Microcephaly protein ANKLE2 promotes Zika virus replication.

Adam T Fishburn¹, Cole J Florio¹, Thomas N Klaessens¹

¹Department of Microbiology and Molecular Genetics, University of California, Davis, California, USA.

|January 13, 2025

Summary

Ankyrin repeat and LEM domain-containing 2 (ANKLE2) protein promotes Zika virus (ZIKV) replication by aiding viral membrane rearrangements. ANKLE2 is essential for ZIKV replication across hosts and contributes to ZIKV-induced microcephaly.

Keywords:

ANKLE2 NS4A Zika virus microcephaly orthoflavivirus virus-host interaction

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Area of Science:

Virology
Molecular Biology
Cell Biology

Background:

Orthoflaviviruses, including Zika virus (ZIKV), replicate by interacting with host proteins.
ZIKV is linked to severe congenital defects like microcephaly, involving the host protein ANKLE2.
Previous work identified an interaction between ZIKV NS4A and ANKLE2, with NS4A inducing microcephaly dependent on ANKLE2.

Purpose of the Study:

To investigate the role of ANKLE2 in ZIKV replication and understand its significance from a viral perspective.
To determine if ANKLE2's role in ZIKV replication is conserved across different hosts and other orthoflaviviruses.

Main Methods:

Examined ANKLE2 localization during ZIKV infection using microscopy.
Assessed ZIKV replication in human and mosquito cell lines with ANKLE2 knockout or knockdown.
Investigated the interaction of ANKLE2 with NS4A from multiple orthoflaviviruses.
Analyzed innate immune activation and endoplasmic reticulum rearrangements in ANKLE2-deficient cells.

Main Results:

ANKLE2 localized to sites of ZIKV NS4A accumulation during infection.
ANKLE2 knockout in human cells significantly reduced ZIKV replication and innate immune activation.
ANKLE2 knockdown in mosquito cells also decreased ZIKV replication.
NS4A proteins from other orthoflaviviruses interacted with ANKLE2 and enhanced their replication.
ANKLE2 knockout cells showed dysregulated virus-induced endoplasmic reticulum rearrangements.

Conclusions:

ANKLE2 is a conserved host factor that promotes orthoflavivirus replication, likely by regulating membrane rearrangements for efficient replication and immune evasion.
The interaction between ZIKV NS4A and ANKLE2 is crucial for viral replication.
ANKLE2's essential role in developing tissues contributes to ZIKV's unique pathogenesis, causing microcephaly.