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Figure 1
Immune Control of Viral Infections
Cellular pattern recognition receptors (PRRs) 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 (IFNα/β). If intrinsic defenses fail to stop virus replication, cytokines and infected cell death
activate sentinel cells (e.g., dendritic cells and 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
(NK) cells, neutrophils, and other granulocytes. Overreaction of this response causes
immunopathology termed a “cytokine storm.” The adaptive, acquired immune response is slow,
systemic, and pathogen specific and leads to the induction of immunological memory. The cellmediated “Th1” response involves the action of CD4+ T helper cells and CD8+ cytotoxic T cells
(CTLs). 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, and 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.