Document Type

Grant

Project Title

Potential roles of the proteins E4 11k and Ddx6 in RIG-I-dependent interferon activation in an adenovirus infection

Principal Investigator

Kasey Karen

Publication Date

Spring 2026

College or Department

Biological & Environmental Sciences

Funder

GCSU AASG

Award Date Range

11/22-5/23

Award Amount

5000

Abstract

Viruses encode many proteins to take over the host cell in order to replicate. There is a constant battle between viruses evolving to combat our immune defenses and host cells evolving to detect and disrupt viral infection. One of the major innate immune defenses against viral infection is the cellular production of interferon, a signaling molecule that can create an antiviral state in the infected cell and surrounding cells. One of the main viral sensors in the cell is RIG-I, which recognizes the double-stranded RNA present during viral infections and activates a signaling cascade that results in interferon beta production. Despite having a double-stranded DNA genome, adenovirus induces a RIG-I-dependent activation of interferon beta due to its expression of virus-associated (VA) RNA1. It is also known that adenovirus expresses a viral protein, E4 11k, that interacts with the cellular protein, Ddx62. It has been shown that some RNA viruses, such as influenza virus, mitigate the RIG-I signaling through Ddx63,4. We aim to determine if the interaction of E4 11k and Ddx6 is involved in regulating the interferon beta antiviral response in the cell. We will use mutant viruses to look at the effect of E4 11k on RIG-I activation and location, and interferon beta production. These studies can contribute to basic biology research to learn more about the role of Ddx6 in RIG-I activation in response to viral infection and possibly lead to new antiviral treatments.

Included in

Biology Commons

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