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Role of RNA helicase DDX1 in influenza A virus replication

Award Number: R15AI159894
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 08/17/2022
PERIOD OF PERFORMANCE END DATE: 07/31/2026

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Role of RNA helicase DDX1 in influenza A virus replication - PROJECT SUMMARY: Influenza virus is a worldwide public health problem and has the potential to cause a pandemic. While vaccines can efficiently protect individuals from infection with influenza virus, there is still a great need for antiviral drugs that prevent disease progression and virus transmission. Thus, efforts are needed to study the influenza virus-host interactions, which are critical for developing novel drugs against the influenza virus, including broad-spectrum drugs. Like other viruses, influenza viruses depend on host cellular components to complete most steps of the viral life cycle. The long-term goal of this project is to identify the critical host cellular proteins that control influenza A virus replication, so that the information can be used for the development of new antiviral drugs. The NS1 protein of influenza virus is a major virulence factor that facilitates influenza virus replication through countering host antiviral response and regulating various processes in virus replication. The NS1 protein exerts these physiological functions largely through interacting with host cellular molecules. Through a quantitative proteomic method, it was recently found that the NS1 protein of influenza A virus interacts with DEAD-box protein 1 (DDX1), a putative DEAD-box-containing RNA helicase. Further preliminary studies demonstrate that knockdown of DDX1 dramatically reduces influenza A virus replication in human lung epithelial cells, suggesting that DDX1 protein is “hijacked” by influenza A virus and functions as a replication cofactor. Concomitantly, knockdown of DDX1 leads to significant decreases in interferon beta mRNA levels in influenza A virus infected cells, suggesting it plays an important role in regulating the transcription of type I interferons. Two specific aims will be pursued in this project. Aim 1. Examine the mechanism by which DDX1 facilitates influenza A virus replication. Aim 2. Examine the mechanisms by which DDX regulates interferon beta expression in influenza A virus-infected cells. The results will contribute to understanding the role of DDX1 in influenza A virus replication and enhance the understanding of influenza virus- host interactions. The results may shed light on designing novel strategies to control influenza viral infection.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2025 ( Subtotal = $0 )
2025	2022	UNIVERSITY OF ARKANSAS	1125 W MAPLE ST STE 316	FAYETTEVILLE	AR	72701	WASHINGTON	USA	Allergy and Infectious Diseases Research	000	1	7/10/2025	NEW	$0
														Subtotal = $0

Issue Date FY: 2022 ( Subtotal = $430,721 )
2022	2022	UNIVERSITY OF ARKANSAS SYSTEM	1125 WEST MAPLE STE 210	FAYETTEVILLE	AR	72701	WASHINGTON	USA	Allergy and Infectious Diseases Research	000	1	8/17/2022	NEW	$430,721
														Subtotal = $430,721

Grand Total All Awards = $430,721

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Role of RNA helicase DDX1 in influenza A virus replication

Award Number: R15AI159894

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 08/17/2022

PERIOD OF PERFORMANCE END DATE: 07/31/2026

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