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Updated: May 21, 2026
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High-throughput Antiviral Assays to Screen for Inhibitors of Zika Virus Replication
Published on: October 30, 2021
Zika virus recruits karyopherin α6 for efficient replication via NS2B
Peixi Chang1, Jia He1, Bhargava Teja Sallapalli1
1Molecular Virology Laboratory, Virginia-Maryland College of Veterinary Medicine, University of Maryland, College Park, Maryland, USA.
Journal of Virology
|May 20, 2026
Summary
Zika virus (ZIKV) hijacks the host cell protein karyopherin α6 (KPNA6) using its NS2B protein. This interaction, crucial for viral replication, relocates KPNA6 to aid ZIKV proliferation.
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Zika virus (ZIKV) caused a major epidemic with severe neurological consequences.
- Mechanisms of ZIKV recruiting host factors for replication are not fully understood.
- Karyopherin α6 (KPNA6) levels increase in ZIKV-infected cells, and its depletion reduces viral replication.
Purpose of the Study:
- To elucidate the interaction between ZIKV and KPNA6.
- To identify the ZIKV protein responsible for KPNA6 relocation.
- To understand how this interaction facilitates ZIKV replication.
Main Methods:
- Confocal microscopy to observe KPNA6 localization.
- Co-immunoprecipitation assays to detect protein-protein interactions.
- Site-directed mutagenesis to identify critical residues for interaction.
Main Results:
- ZIKV infection causes KPNA6 to relocate to the perinuclear region, co-localizing with viral RNA.
- The ZIKV protein NS2B mediates KPNA6 relocation and interacts with KPNA6.
- Specific residues (P115, G119) in NS2B are essential for KPNA6 interaction and ZIKV replication.
Conclusions:
- ZIKV utilizes its NS2B protein to induce KPNA6 relocation, a novel host-pathogen interaction.
- This interaction recruits the host proviral factor KPNA6 to promote viral proliferation.
- Understanding this mechanism offers potential targets for antiviral strategies against ZIKV.
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