Viral infection of the lung: host response and sequelae

Abstract

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.

Keywords: AIM2; APC; ASC; Absent in melanoma 2; Antigen-presenting cell; Apoptosis-associated speck-like protein containing CARD; B-cell immunity; CTL; Cytotoxic CD8(+) T-cell; DAMP; DC; Damage-associated molecular pattern; Dendritic cell; Follicular helper T; GC; Germinal center; HMGB1; High-mobility group box 1; IAV; ILC; ILC-II; IRF; Influenza A virus; Innate lymphoid cell; Interferon regulatory factor; LAPC; Late activator antigen-presenting cell; MAVS; MLN; Mediastinal lymph node; Mitochondrial anti-viral signaling; NK; NLRP3; Natural killer; Nod-like receptor family protein 3; PAMP; PRR; Pathogen-associated molecular pattern; Pattern recognition receptor; RIG-I; RIG-I–like receptor; RLR; RSV; Regulatory T; Respiratory syncytial virus; Retinoic acid–inducible gene I; T(FH); T-cell immunity; TLR; Toll-like receptor; Treg; Type II innate lymphoid cell; Viral sensor molecules; adaptive immunity; innate immunity; stem cells; tissue repair; viral clearance.