| Summary: | Influenza A virus is a serious public health threat. Most recently the 2009/H1N1 pandemic virus had an inherent ability to evade the host's immune surveillance
through genetic drift, shift, and genomic reassortment. Immune characterization of 2009/H1N1 utilized monoclonal antibodies, neutralizing sera, and proteomics.
Increased age may have provided some degree of immunity, but vaccines against seasonal influenza viruses seldom yield cross-reactive immunity, exemplified by
2009/H1N1. Nonetheless, about 33% of individuals, over the age of 60, had cross-reactive neutralizing antibodies against 2009/H1N1, whereas only 6-9% young
adults had these antibodies. Children characteristically had no detectable immunity against 2009/H1N1. Taken together, these observations suggest some degree of
immune transference with at least certain strains of virus that have afflicted the human population in past decades. Because internal influenza proteins may exhibit
less antigenic variation, it is possible that prior exposure to diverse strains of influenza virus provide some immunity to novel strains, including the recent
pandemic strain (swine-avian A/H1N1). Current trends in immunological studies – specifically the modulation of cellular immune surveillance provided by TH17
and Tregs – also support the need for additional proteomic research for characterizing novel translational evidence-based treatment interventions based on cytokine
function to help defeat the virus. Timely and critical research must characterize the impact of genetics and epigenetics of oral and systemic host immune
surveillance responses to influenza A virus. The continued development and application of proteomics and gene expression across viral strains and human tissues
increases our ability to combat the spread of influenza epidemics and pandemics.
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