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.

Understanding Interferon Subtype Therapy for Viral Infections: Harnessing the Power of the Innate Immune System.

“…Therefore Manipulating the immune system through exogenous cytokine delivery, in the absence of the viral insult, should be heeded with caution as interfering with host immunity may generate long-term inflammatory side effects. The main goal is to achieve full protection by initiating immune responses against the virus-infected targets with the subsequent inflammatory responses returning to baseline levels, restoring homeostasis in tissues and organs [62], as unresolved inflammation with disturbed baselines post virus infection may perpetuate chronic inflammatory disease [63]. On a cautionary note, there are important implications for potential therapeutic use of IFNs in acute versus chronic virus infections.…”

STAT4 Deficiency Fails To Induce Lung Th2 or Th17 Immunity following Primary or Secondary Respiratory Syncytial Virus (RSV) Challenge but Enhances the Lung RSV-Specific CD8 + T Cell Immune Response to Secondary Challenge

“…Type I interferons and IL-27 are STAT1-activating cytokines that promote antiviral host defense and regulate inflammation through a variety of pathways (66,67). To determine whether STAT4 Ϫ/Ϫ mice had increased expression levels of each of these cytokines at early time points following primary RSV challenge, we measured IFN-␣, IFN-␤, and IL-27 protein levels in lungs of RSV-challenged mice by ELISAs at 12 and 24 h postinfection.…”

The Suppressive Effect of Quercetin on Toll-Like Receptor 7-Mediated Activation in Alveolar Macrophages

“…Viral respiratory tract infections cause pneumonia and exacerbations of chronic lung diseases, such as asthma [1] . The airway epithelial cells, alveolar macrophages (AMs), and dendritic cells recognize the component of an invading virus through host pattern-recognition receptors.…”

“…The airway epithelial cells, alveolar macrophages (AMs), and dendritic cells recognize the component of an invading virus through host pattern-recognition receptors. After recognition of viral components, pattern-recognition receptors initiate an efficient antiviral response and trigger a specific adaptive immune response [1][2][3][4] .…”