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Updated: Jun 2, 2026

Affinity Purification of Influenza Virus Ribonucleoprotein Complexes from the Chromatin of Infected Cells
Published on: June 3, 2012
Nrf2 expression modifies influenza A entry and replication in nasal epithelial cells
Matthew J Kesic1, Steven O Simmons, Rebecca Bauer
1Curriculum in Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7127, USA. kesic@email.unc.edu
The antioxidant pathway Nrf2 (Nuclear factor erythroid 2-related factor 2) significantly impacts influenza virus replication. Activating Nrf2 with antioxidants like SFN and EGCG inhibits viral entry and replication in human nasal cells.
Area of Science:
- * Cellular and Molecular Biology
- * Immunology
- * Virology
Background:
- * Influenza virus poses a significant global health threat, causing widespread morbidity and mortality.
- * Antioxidant pathways, particularly those involving Nrf2 (Nuclear factor erythroid 2-related factor 2), are implicated in inflammation and immune responses.
- * The precise role of Nrf2-dependent gene expression in viral susceptibility and clearance remains to be fully elucidated.
Purpose of the Study:
- * To investigate the mechanistic role of Nrf2-dependent gene expression in regulating influenza virus entry and replication.
- * To determine the effect of Nrf2 activation and inhibition on viral susceptibility in human nasal epithelial cells (NEC).
Main Methods:
- * Utilized differentiated human NEC and an enzymatic virus-like particle entry assay.
- * Employ lentiviral vectors expressing Nrf2-specific short hairpin (sh)-RNA to knockdown Nrf2 expression.
- * Administered Nrf2 activators, sulforaphane (SFN) and epigallocatechin gallate (EGCG), to assess their impact on viral replication.
Main Results:
- * Nrf2 knockdown significantly increased influenza virus entry and replication in human NEC.
- * Supplementation with SFN and EGCG markedly decreased viral entry and replication.
- * EGCG's suppressive effect on viral replication was abolished in Nrf2-knockdown cells, confirming a causal link.
- * Nrf2 activation by SFN and EGCG upregulated baseline antiviral mediators (RIG-I, IFN-β, MxA).
Conclusions:
- * Nrf2-dependent gene expression exhibits an inverse relationship with influenza virus entry and replication.
- * Nrf2-activating antioxidants inhibit viral replication in human NEC, suggesting a potential therapeutic strategy.
- * Nrf2 activation enhances innate antiviral responses, contributing to host defense against influenza.
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