The interferon (IFN) response is well-established to be a major determinant of pathogenesis in many viral systems. Not surprisingly, viruses have evolved many and diverse mechanisms to inhibit the IFN response and its downstream effector molecules (IFN stimulated genes; ISGs). Our goal is to identify and characterize interactions between viruses and host immune molecules (ISGs) that contribute to the development of pathogenesis. In particular, our research is focused on understanding how viral RNA functions to modulate these virus-host interactions, and aims to address questions such as:
How do changes in viral RNA sequence and structure impact virus-host interactions and pathogenesis?
How do changes in viral RNA impact nucleic acid sensing by the host?
What is the molecular mechanism(s) of ISGs that impact viral pathogenesis?
What mechanisms have viruses evolved to circumvent restriction by these host factors?
Hickson, S, Brekke, E, Schwerk J, Salukhe, N, Zaver, S, Woodward, J, Savan, R, Hyde JL. Sequence diversity in the 3’ untranslated region of alphavirus modulatesIFIT2-dependent restriction in a cell type dependent manner. Review Commons (in review), 2021.
Soveg FW, Schwerk J, Gokhale NS, Cerosaletti K, Smith JR, Pairo-Castineira E, Kell AM, Forero A, Zaver SA, Esser-Nobis K, Roby JA, Hsiang TY, Ozarkar S, Clingan JM, McAnarney ET, Stone AE, Malhotra U, Speake C, Perez J, Balu C, Allenspach EJ, Hyde JL, Menachery VD, Sarkar SN, Woodward JJ, Stetson DB, Baillie JK, Buckner JH, Gale M Jr, Savan R. Endomembrane targeting of human OAS1 p46 augments antiviral activity. Elife. 2021 Aug 3;10. doi: 10.7554/eLife.71047. PubMed PMID: 34342578.