1 August 2013
Viral sensor molecules, innate immunity, adaptive immunity, T-cell immunity, B-cell immunity, viral clearance, tissue repair, stem cells, AIM2, Absent in melanoma 2, APC, Antigen-presenting cell, ASC, Apoptosis-associated speck-like protein containing CARD, CTL, Cytotoxic CD8+ T-cell, DAMP, Damage-associated molecular pattern, DC, Dendritic cell, GC, Germinal center, HMGB1, High-mobility group box 1, IAV, Influenza A virus, ILC, Innate lymphoid cell, ILC-II, Type II innate lymphoid cell, IRF, Interferon regulatory factor, LAPC, Late activator antigen-presenting cell, MAVS, Mitochondrial anti-viral signaling, MLN, Mediastinal lymph node, NK, Natural killer, NLRP3, Nod-like receptor family protein 3, PAMP, Pathogen-associated molecular pattern, PRR, Pattern recognition receptor, RIG-I, Retinoic acid–inducible gene I, RLR, RIG-I–like receptor, RSV, Respiratory syncytial virus, TFH, Follicular helper T, TLR, Toll-like receptor, Treg, Regulatory T
Because of its essential role in gas exchange and oxygen delivery, the lung has evolved a variety of strategies to control inflammation and maintain homeostasis. Invasion of the lung by pathogens (and in some instances exposure to certain noninfectious particulates) disrupts this equilibrium and triggers a cascade of events aimed at preventing or limiting colonization (and more importantly infection) by pathogenic microorganisms. In this review we focus on viral infection of the lung and summarize recent advances in our understanding of the triggering of innate and adaptive immune responses to viral respiratory tract infection, mechanisms of viral clearance, and the well-recognized consequences of acute viral infection complicating underlying lung diseases, such as asthma.