The Horner Lab
Studying RNA Virus - Host Interactions
RNA Biology, Cell Biology, Antiviral Innate Immunity
Welcome to the Horner lab!
Our research goal is to define the virus-host interactions that control the outcome of infection to hepatitis C virus and other Flaviviridae, including dengue virus and Zika virus. We hope to define the molecular mechanisms of how these viruses activate and evade host innate immune defenses, as well as RNA regulatory controls to viral infection and immunity. In particular, we are interested in the cell biological, post-translational, and post-transcriptional controls that regulate viral infection. As we carry out this research, we aim to train the next generation of scientist
Our lab is located at Duke University in the School of Medicine in Durham, NC in the Department of Integrative ImmunoBiology. We are members of the Center for RNA Biology, Center for Virology, Center for Host-Microbial Interactions, and Epigenetics & Epigenomics Program.
Recent Publications
Transcript architecture sets the m6A landscape: CSTF2 and CSTF2T reshape m6A through cleavage-dependent and -independent mechanisms. doi: 10.64898/2026.03.27.714597.
IFIT3 Associates with m6A-Modified RNA to Restrict Hepatitis C Virus Infection. doi: 10.64898/2026.03.25.714224.
The m6A methyltransferase complex protein VIRMA engages hepatitis C virus RNA through a WTAP-independent mechanism. doi: 10.64898/2026.09.11.750944:2026.09.11.750944.
UFMylation promotes orthoflavivirus infectious particle production. doi: 10.1101/2025.01.09.632082
Signaling from the RNA sensor RIG-I is regulated by ufmylation. doi: 10.1073/pnas.2119531119
14-3-3ϵ UFMylation promotes RIG-I-mediated signaling. doi: 10.1101/2025.03.19.644084.