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Influenza Virus Hijacks Body’s Gene Regulation to Enhance Spread

Research from the University of Gothenburg reveals that the influenza virus exploits the body’s gene regulation mechanisms to promote its transmission. The findings suggest that a drug already on the market might bolster immune responses, although further validation in humans is necessary.

The research, detailed in a recent publication in Nucleic Acids Research, uncovers a previously unrecognized tactic employed by the influenza A virus. It shows how the virus manipulates a specific protein, critical for regulating gene activity, to undermine the immune response.

Known as AGO2, this protein plays a key role in RNA interference, a biological process that controls which genes are expressed within cells. Typically, AGO2 functions outside the cell nucleus, but during viral infection, the flu virus shifts the protein into the nucleus, where it silences genes pivotal for immune defense.

Disabling Immune Alerts

This research primarily focuses on type I interferons—molecules used by infected cells to signal neighboring cells and fortify the body’s defenses.

Aishe Sarshad, an associate professor at Sahlgrenska Academy and one of the senior authors, commented on the significance of the findings: “It’s astonishing that the virus can commandeer such a fundamental and intricately regulated system as RNA interference, especially within the nucleus where AGO2 is typically absent.”

Much of the experimental work was conducted by Hsiang-Chi Huang, who was a postdoctoral fellow in the research group during the study. The findings demonstrate that AGO2 follows the tumor suppressor protein p53 into the nucleus, attaching to genes that manage the body’s alarm signals and effectively turning them off.

Potential for New Antiviral Treatments

The researchers also explored whether the viral manipulation could be counteracted. They tested arsenic trioxide (ATO), a medication approved for treating a specific type of blood cancer. In experiments conducted on cell cultures and mice, ATO was effective in enhancing interferon production and diminishing the viral load in the lungs.

This suggests a promising avenue for harnessing the body’s own RNAi system to impede viral infections, potentially extending this strategy beyond influenza to other RNA-based viruses as well.

“We aim to continue our research to determine if this same mechanism operates in different infections. This could lead to a novel class of antiviral therapies that target not only the virus itself but also how it exploits our cellular machinery,” said Sarshad.

More information: Hsiang-Chi Huang et al, Nuclear AGO2 supports influenza A virus replication through type-I interferon regulation, Nucleic Acids Research (2025). DOI: 10.1093/nar/gkaf268

Citation: How the influenza virus hijacks cell machinery to suppress immune alarm signals (2025, April 28) retrieved 28 April 2025 from https://phys.org/news/2025-04-influenza-virus-hijacks-cell-machinery.html

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