ABSTRACT
Infl uenza A virus (IAV) presents an ongoing major threat to human health and there is much yet to be learned about the role of innate immunity during IAV infection (Tripathi et al. 2015). Although IAV elicits strong adaptive immune responses, it is prone to rapid genomic variation either through small incremental mutations or major changes resulting from exchange of genome segments with those of animal strains (reassortment). These genomic changes allow IAV to escape immune responses generated against prior strains. Generally the small incremental changes lead to seasonal epidemics, whereas reassortment leads to pandemics. The presence of animal reservoirs allows introduction of avian or pig strains (or genes from these strains) into humans resulting in pandemics, as in 2009 (Dawood et al. 2009). Seasonal epidemics of infl uenza virus still contribute tremendous morbidity and mortality including annual mortality in the USA of ~40,000 (Morens 2003). Certain groups of individuals are more susceptible to severe outcomes of seasonal IAV: those at extremes of age, smokers, individuals with chronic obstructive pulmonary disease (COPD), cystic fi brosis or asthma, diabetes mellitus, cardiovascular disease, or immune compromise. Some otherwise healthy young people die during seasonal epidemics, sometimes due to bacterial super-infection (e.g., note recent association of IAV with MRSA pneumonia) (Hartshorn 2010). Pandemics cause more indiscriminate mortality in young healthy adults than seasonal IAV (Hartshorn 2013). There is a period of 5-7 days prior to arrival of CD8+ T cells in the lung after exposure to a new IAV strain and innate defense is critical at this time. The innate immune response to IAV is highly complex and this chapter will focus on the initial phase of the response in respiratory tract.
