Influenza Lung Immunology: Major Aspects

Influenza causes an acute infection of the host and initiates a cascade of immune reactions activating almost all parts of the immune defense system. Most of the initial innate response, including cytokine release (IFNα/β), influx of neutrophil granulocytes or natural killer cells, and cell activation, is responsible for the acute onset of the clinical symptoms. Innate immunity is an essential prerequisite for the adaptive immune response, firstly, to limit the initial viral replication and antigen load, and secondly, because the antigen-specific lymphocytes of the adaptive immune response are activated by co-stimulatory molecules that are induced on cells of the innate immune system during their interaction with viruses. Influenza viruses, however, encode in the non-structural protein 1 (NS1) mechanisms to evade and antagonize the IFN α/β response. NS1 is likely to sequester viral dsRNA which prevents recognition of this dangerous molecule by cellular sensors which would otherwise trigger IFN α/β release.

Evasion from the host immune response requires a lot of viral proteins to associate with and inhibit cellular proteins with antiviral functions. Because viral genomes are typically 10,000 to 100,000 times smaller than the human genome, most or all steps of virus infection depend on exploiting host gene functions. Identifying such host genes is currently a crucial frontier in understanding infection. These host genes also are attractive targets for viral control, since they are not subject to the high mutation rates by which viruses escape from antivirals targeted against their own genes.

  • Pathogenesis and immunology
  • Humoral immune response
  • T cell memory in the lung airways
  • Development of airway reactivity to nitrates in subjects with influenza
  • Anatomical features of anti-viral immunity in the respiratory tract
  • Attenuated influenza produced by experimental intranasal inoculation
  • Other respiratory infections

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