Since the host immune system deteriorates significantly during aging, the inability to generate effective, broad-spectrum immune memory following infection or vaccination contributes to increased influenza burden among the elderly ( Bridges et al., 2000 Castle, 2000 Dao et al., 2010 Thompson et al., 2003). During the 2012-2013 season, persons aged ≥ 65 years accounted for ∼50% of all influenza-related hospitalizations in the US (Centers for Disease Control and Prevention (CDC), 2013). The elderly influenza disease rate in humans carries a heavy burden on healthcare systems and perpetuates virus circulation in the general population. With the presence of an aged model, dissecting clinical morbidity, viral dynamics and immune response during influenza infection will aid the development of future prophylactics such as age specific influenza vaccines. These results revealed dampened immune activation during sequential influenza infection in aged ferrets. Furthermore, increased clinical morbidity was associated with slower and shorter hemagglutinin antibody generation and attenuated type 1 T-cell gene responses in peripheral blood. Our findings demonstrated experimentally that aged ferrets had significant morbidity during monosubtypic heterologous 2° challenge with significant weight loss and respiratory symptoms. To better represent the immune environment, we investigated clinical morbidity and immune function during sequential homologous and heterologous H1N1 influenza infection in an aged ferret model. The challenge managing influenza-associated illness in the elderly is the decline of immune function, where mechanisms leading to immunological senescence have not been elucidated. The major burden of influenza morbidity resides within the elderly population.
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