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ARS Home » Plains Area » Manhattan, Kansas » Center for Grain and Animal Health Research » ABADRU » Research » Publications at this Location » Publication #408485

Research Project: Predicting and Mitigating Vesicular Stomatitis Virus (VSV) in North America

Location: Arthropod-borne Animal Diseases Research

Title: Vesicular stomatitis virus elicits early transcriptome response in Culicoides sonorensis cells

item Scroggs, Stacey
item BIRD, EDWARD - Kansas State University
item Molik, David
item Nayduch, Dana

Submitted to: Viruses
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/13/2023
Publication Date: 10/18/2023
Citation: Scroggs, S.L., Bird, E.J., Molik, D.C., Nayduch, D. 2023. Vesicular stomatitis virus elicits early transcriptome response in Culicoides sonorensis cells. Viruses. 10.3390/v15102108.

Interpretive Summary: Vesicular stomatitis is a viral disease transmitted to livestock by biting midges, black flies, and sand flies. The molecular interactions between vesicular stomatitis virus (VSV) and the vectors are not well understood. We infected a midge cell line with VSV and collected cellular lysates at multiple time points for transcriptome sequencing. The transcriptome of VSV-infected cells differed from the uninfected controls only at 1 hour post infection (HPI) and not at the later time points. Additionally, several immune response related genes were up or down regulated with VSV infection. Our work suggests that VSV vector competence of biting midges may be related to their immune response or lack thereof.

Technical Abstract: Viruses that are transmitted by arthropods, or arboviruses, have evolved to successfully navigate both the invertebrate and vertebrate hosts, including their immune systems. Biting midges transmit several arboviruses including vesicular stomatitis virus (VSV). To study the interaction be-tween VSV and midges, we characterized the transcriptomic responses of VSV-infected and mock infected Culicoides sonorensis cells at 1, 8, 24, and 96 hours post infection (HPI). The tran-scriptomic response of VSV-infected cells at 1 HPI was significant, but by 8 HPI there were no de-tectable differences between the transcriptome profiles of VSV-infected and mock infected cells even though viral replication remained high. Several genes involved in immunity were upregulated (ATG2B and TRAF4) or downregulated (SMAD6 and TOLL7) in VSV-treated cells at 1 HPI. These results indicate that VSV infection in midge cells produces an early immune response that quickly wanes, giving insight into in vivo C. sonorensis VSV tolerance that may underlie their permissiveness as vectors for this virus.