Interplay between innate immunity and negative-strand RNA viruses: towards a rational model

Area of Science:

• Immunology
• Virology
• Molecular Biology

Background:

• RIG-like receptors (RLRs) are crucial cytosolic sensors of viral RNA.
• RLR activation triggers type I interferon (IFN) production, initiating innate immune responses.
• Existing reviews often focus narrowly on RLR signaling or viral inhibition of IFN, lacking a comprehensive view.

Purpose of the Study:

• To integrate knowledge of RLR signaling with the virus replication cycle.
• To address discrepancies between cell-intrinsic innate immunity models and virus biology, particularly for Mononegavirales.
• To build a more relevant model of the interplay between Mononegavirales and the innate immune system.

Main Methods:

• Literature review and synthesis of existing research on RLRs, innate immunity, and Mononegavirales.
• Comparative analysis of RLR signaling pathways and viral replication strategies.
• Identification of knowledge gaps and discrepancies in current models.

Main Results:

• RLR agonists, signal transduction, and regulators of IFN immunity have been extensively studied.
• Viral proteins are known inhibitors of the innate immune response.
• Discrepancies exist between established innate immunity models and the biology of viruses like Mononegavirales.

Conclusions:

• A unified understanding of RLRs, innate immunity, and virus replication is needed.
• Reconciling virology and innate immunity is essential for accurate modeling of host-pathogen interactions.
• This review provides a framework for developing improved models for Mononegavirales and innate immunity.