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. Author manuscript; available in PMC: 2014 Apr 17.
Published in final edited form as: Cell Host Microbe. 2013 Apr 17;13(4):379–393. doi: 10.1016/j.chom.2013.03.010

Figure 1. Immune Control of Viral Infections.

Figure 1

Cellular pattern recognition receptors (PRR) recognize viral molecules after attachment and entry. This initial recognition starts a cell autonomous intrinsic defense involving increased synthesis of many antiviral proteins, and several cytokines, including type I interferons (IFN-α/β). If intrinsic defenses fail to stop virus relication, cytokines and infected cell death activate sentinel cells (e.g. dendritic cells, macrophages), which produce copious cytokines and present antigens to trigger T-cell mediated immunity. The innate immune response, which is activated quickly and robustly, also involves the actions of the complement system, natural killer cells (NK), neutrophils and other granulocytes. Over-reaction of this response causes immunopathology termed a “cytokine storm”. The adaptive, acquired immune response is slow, systemic, pathogen-specific, and leads to the induction of immunological memory. The cell-mediated “Th1” response involves the action of CD4+ T-helper cells and CD8+ Cytotoxic T-cells (CTL). CTLs are important to kill infected cells and to produce type II interferon (IFN-γ) and tumor necrosis factor (TNF-α).The “Th2” humoral response involves CD4+ T-helper cells and antibody-producing B-cells. Most of the time, the clinical symptoms of virus infection (e.g. fever, pain, tissue damage) are caused by the inflammatory action of the innate and adaptive immune systems. Due to their mostly irreplacable nature, nervous system tissues rely predominantly on the intrinsic and innate immune responses, and avoid the extensive inflammation and cytotoxic effects of the adaptive immune response.