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Identification of RNAi-independent antiviral genes through biased genetic screen in C. elegans

Award Number: R21AI188074
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: 02/02/2026
PERIOD OF PERFORMANCE END DATE: 01/31/2028

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Identification of RNAi-independent antiviral genes through biased genetic screen in C. elegans - PROJECT SUMMARY Viruses, especially RNA viruses, are formidable pathogens to cellular hosts. Owing to the error-prone nature of their replicases, RNA viruses rapidly accumulate large numbers of genetic mutations in their genome, enabling them to evade immune detection. Some RNA viruses, such as influenza viruses and coronaviruses, can also generate genome variants through genome reassortment or genome recombination mechanisms. It is thus important to study antiviral mechanisms intrinsically resistant to genetic mutations in viral genome, which may lead to the development of novel antiviral strategies. In plants, insects and vertebrates, there are antiviral mechanisms triggered by non-dsRNA products of invading viruses. These antiviral mechanisms provide another layer of protection in case viral dsRNA-triggered immunity is compromised by the invading viruses. In supporting this hypothesis, many plant and animal viruses have been found to produce diverse types of dsRNA binding proteins that are able to bind and sequester viral dsRNA to block immune detection. So far, RNAi is known as the most important antiviral defense mechanism in Caenorhabditis elegans. However, some recent studies on worm antiviral defense suggest that viral infection in C. elegans triggers transcriptional programs that in return provide protection against invading viruses in an RNAi-independent manner. Therefore, very much like what has been demonstrated in plants and insects, RNAi-independent antiviral defense (RiAD) may provide worms another layer of protection against virus in case antiviral RNAi is compromised. To fill the knowledge gap in our understanding of worm RiAD and as proof of principle, the PI’s lab has recently carried out a biased genetic screen of limited scale, aiming to identify genes specifically contributing to worm RiAD. This genetic screen identified 8 candidate genes that confer RiAD targeting a flock house virus (FHV) replicon. 5 of these candidate genes also mediate RiAD against Orsay virus, which naturally infects C. elegans (21). In this application, we propose to continue the biased genetic screen and finish it on a much greater scale to ensure double coverage on all genes involved in RiAD. We will then map and identify the candidate genes through whole genome sequencing combined with feeding RNAi and function rescue assay. Since approximately 70% of C. elegans genes have human homologs, function and mechanism study of the identified genes may not only lead to the identification of novel conserved mechanisms of antiviral innate immunity across kingdoms but also inform the development of novel antiviral strategies.


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: 2026 ( Subtotal = $412,500 )
2026	2026	LOUISIANA STATE UNIVERSITY	202 HIMES HALL	BATON ROUGE	LA	70803	EAST BATON ROUGE	USA	Allergy and Infectious Diseases Research	000	1	2/2/2026	NEW	$412,500
														Subtotal = $412,500

Grand Total All Awards = $412,500

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Identification of RNAi-independent antiviral genes through biased genetic screen in C. elegans

Award Number: R21AI188074

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: 02/02/2026

PERIOD OF PERFORMANCE END DATE: 01/31/2028

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