Details

Autor(en) / Beteiligte

• Linder, Andreas
• Bothe, Viktoria
• Linder, Nicolas
• Schwarzlmueller, Paul
• Dahlström, Frank
• Bartenhagen, Christoph
• Dugas, Martin
• Pandey, Dharmendra
• Thorn-Seshold, Julia
• Boehmer, Daniel F R
• Koenig, Lars M
• Kobold, Sebastian
• Schnurr, Max
• Raedler, Johannes
• Spielmann, Giulia
• Karimzadeh, Hadi
• Schmidt, Andreas
• Endres, Stefan
• Rothenfusser, Simon

Titel

Defective Interfering Genomes and the Full-Length Viral Genome Trigger RIG-I After Infection With Vesicular Stomatitis Virus in a Replication Dependent Manner

Ist Teil von

• Frontiers in immunology, 2021-04, Vol.12, p.595390

Ort / Verlag

Switzerland: Frontiers Media S.A

Erscheinungsjahr

2021

Quelle

MEDLINE

Beschreibungen/Notizen

• Replication competent vesicular stomatitis virus (VSV) is the basis of a vaccine against Ebola and VSV strains are developed as oncolytic viruses. Both functions depend on the ability of VSV to induce adequate amounts of interferon-α/β. It is therefore important to understand how VSV triggers interferon responses. VSV activates innate immunity retinoic acid-inducible gene I (RIG-I), a sensor for viral RNA. Our results show that VSV needs to replicate for a robust interferon response. Analysis of RIG-I-associated RNA identified a copy-back defective-interfering (DI) genome and full-length viral genomes as main trigger of RIG-I. VSV stocks depleted of DI genomes lost most of their interferon-stimulating activity. The remaining full-length genome and leader-N-read-through sequences, however, still triggered RIG-I. Awareness for DI genomes as trigger of innate immune responses will help to standardize DI genome content and to purposefully deplete or use DI genomes as natural adjuvants in VSV-based therapeutics.