The Homeostasis of Host Innate Immunity and Virus Infection

The homeostasis of host innate immunity and virus infection is critically dependent on the cellular immune response. Viral infection activates the immune response of host cells, and pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs) and other intracellular receptors like RIG-I-like receptors (RLRs) and NOD-like receptors (NLRs), are involved in this process. These receptors recognize characteristic molecular patterns of viruses, such as viral RNA or viral proteins, which initiate intracellular signal transduction pathways. In this process, host cells are prompted to release various inflammatory factors, including interferons (IFNs), tumor necrosis factor-alpha (TNF-α), and interleukins (ILs). These factors not only directly inhibit viral replication, but also enhance overall immune defenses by activating the antiviral status of neighboring cells. However, excessive inflammatory responses may lead to cellular damage, tissue destruction, and systemic disease. Therefore, host cells control the inflammatory response by producing inhibitory cytokines such as interleukin-10 (IL-10) and transforming growth factor beta (TGF-β), and by recruiting regulatory immune cells such as regulatory T cells (Tregs). These mechanisms work together to ensure a balanced immune response and to prevent autoimmune disease or chronic inflammation that can be triggered by immune overactivity.

The purpose of maintaining immune homeostasis is to effectively control the spread of the virus while protecting the host from immune-mediated damage. Dysregulation of this balance may lead to the persistence of viral infection or an overreaction of the immune system, thereby affecting the health status of the host. Precise modulation of the immune response can inhibit viral replication and clear infection while avoiding triggering severe tissue inflammation and damage. Investigating the mechanisms that regulate the host immune response is critical to understanding the pathology of viral infections and developing effective therapeutic strategies. Through in-depth exploration of immune regulation during viral infection, crucial immune regulators can be identified, facilitating the design of more targeted antiviral drugs or immunomodulatory therapies.

We welcome Mini-Reviews, full-length Reviews, and Original Research papers. Our Research Topic includes, but is not necessarily limited to:
• Host Immune Response and Virus Infection: Mechanisms of immune recognition, initial antiviral responses, and adaptive immunity activation in virus infections.
• Virus Evasion and Persistence: Mechanisms of virus escape, including mutations and immune signaling inhibition, and the persistence of viral infections and their effects on the host.
• Regulatory Immune Mechanisms: Negative feedback and regulatory immune cell actions, as well as the role of novel immunoregulatory molecules in virus infections.
• Clinical and Interdisciplinary Research: Clinical research on virus infections and the integration of systems biology, computational biology, and clinical data to understand host-virus interactions.

Keywords: virus, host, infection, hemeostasis

Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.