Regulation of antiviral innate immune signaling and viral evasion following viral genome sensing

Abstract

A harmonized balance between positive and negative regulation of pattern recognition receptor (PRR)-initiated immune responses is required to achieve the most favorable outcome for the host. This balance is crucial because it must not only ensure activation of the first line of defense against viral infection but also prevent inappropriate immune activation, which results in autoimmune diseases. Recent studies have shown how signal transduction pathways initiated by PRRs are positively and negatively regulated by diverse modulators to maintain host immune homeostasis. However, viruses have developed strategies to subvert the host antiviral response and establish infection. Viruses have evolved numerous genes encoding immunomodulatory proteins that antagonize the host immune system. This review focuses on the current state of knowledge regarding key host factors that regulate innate immune signaling molecules upon viral infection and discusses evidence showing how specific viral proteins counteract antiviral responses via immunomodulatory strategies.

Immunology: Viral infection and host defenses

In the initial stages of viral infection, the body relies on innate or non-specific immune signaling pathways to spur antiviral response mechanisms into action, however viruses have evolved to counteract these defense mechanisms. Jong-Soo Lee and colleagues from Chungnam National University in Daejeon, South Korea, review the signaling pathways and regulatory factors involved in these two opposing processes. The researchers detail the different molecular players involved in recognizing DNA or RNA from viruses and highlight the immune-modulating mechanisms by which viruses evade detection. A more complete knowledge of these pathways and their interactions could help drug developers identify new ways of treating or preventing viral infections. It could also provide insights into how autoimmunity and other problems can arise when these antiviral surveillance mechanisms fail to work correctly.