Influenza 2009 pandemic: Cellular immune-mediated surveillance modulated by TH17 & Tregs 


Andre Barkhordarian1*, Natasha Iyer1, Paul Shapshak2, 3, Charurut Somboonwit2, 4, John Sinnott2, 4, Francesco Chiappelli1 


1Division of Oral Biology & Medicine, Section of Oral Biology, UCLA School of Dentistry, Los Angeles, CA 90095; 2Division of Infectious Disease and International Medicine, Tampa General Hospital, College of Medicine, University of South Florida, Tampa, FL; 3Department of Psychiatry and Behavioral Medicine, College of Medicine, University of South Florida, Tampa, FL; 4Hillsborough Florida Health Department, Tampa, FL 

Email; *Corresponding author

Article Type

Current trends



Received February 14, 2011; Accepted February 16, 2011; Published March 02, 2011



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.  


A/H1N1 2009, cytokines, TH17, Tregs, cellular immunity, epigenetics, comparative effectiveness and efficacy research 


Barkhordarian et al. Bioinformation 6(1): 39-40 (2011)

Edited by

P Kangueane






Biomedical Informatics



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