RNA modification in immune evasion and immune recognition

• Applicant: Professor Dr. Stefan Bauer
• Subject Area: Immunology
• Term: from 2009 to 2012
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 115690894

The innate immune system senses viral RNA via Toll-like receptors (TLR) and RNA helicases. RNA modifications such as 2’O-ribosemethylation or base methylation (5-methyl-cytidine) render self RNA non-immunostimulatory and are the basis of selfversus viral RNA discrimination. However, the role of self or viral RNA in immunoregulation and immune evasion are not well understood. We have demonstrated that non-modified RNA triggers TLR7, whereas 2’O-ribose methylated RNA blocks immune activation. It is hypothesized that certain RNA viruses methylate their genome by virally encoded 2’O-ribose-methyltransferase (2’O-MTase) to evade immune recognition. Furthermore, our data suggest that viral infection or in vitro digestion with single-strand-specific RNase A renders self RNA immunostimulatory. The goal of the project is to discover and define novel basic viral and host immune mechanisms. They will provide a more sophisticated understanding of the immune response to virus infection and may lead to new adjuvant for future vaccine and therapeutic antiviral drug development.

• DFG Programme: Research Grants