Influenza 2009 pandemic: Cellular immunemediated surveillance modulated by TH17 & Tregs

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, neutralizi...

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Main Authors:	Barkhordarian, Andre, Iyer, Natasha, Shapshak, Paul, Somboonwit, Charurut, Sinnott, John, Chiappelli, Francesco
Format:	Online
Language:	English
Published:	Biomedical Informatics 2011
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3064851/

id	pubmed-3064851
recordtype	oai_dc
spelling	pubmed-30648512011-04-04 Influenza 2009 pandemic: Cellular immunemediated surveillance modulated by TH17 & Tregs Barkhordarian, Andre Iyer, Natasha Shapshak, Paul Somboonwit, Charurut Sinnott, John Chiappelli, Francesco Current Trends 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. Biomedical Informatics 2011-03-02 /pmc/articles/PMC3064851/ /pubmed/21464844 Text en © 2011 Biomedical Informatics This is an open-access article, which permits unrestricted use, distribution, and reproduction in any medium, for non-commercial purposes, provided the original author and source are credited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Barkhordarian, Andre Iyer, Natasha Shapshak, Paul Somboonwit, Charurut Sinnott, John Chiappelli, Francesco
spellingShingle	Barkhordarian, Andre Iyer, Natasha Shapshak, Paul Somboonwit, Charurut Sinnott, John Chiappelli, Francesco Influenza 2009 pandemic: Cellular immunemediated surveillance modulated by TH17 & Tregs
author_facet	Barkhordarian, Andre Iyer, Natasha Shapshak, Paul Somboonwit, Charurut Sinnott, John Chiappelli, Francesco
author_sort	Barkhordarian, Andre
title	Influenza 2009 pandemic: Cellular immunemediated surveillance modulated by TH17 & Tregs
title_short	Influenza 2009 pandemic: Cellular immunemediated surveillance modulated by TH17 & Tregs
title_full	Influenza 2009 pandemic: Cellular immunemediated surveillance modulated by TH17 & Tregs
title_fullStr	Influenza 2009 pandemic: Cellular immunemediated surveillance modulated by TH17 & Tregs
title_full_unstemmed	Influenza 2009 pandemic: Cellular immunemediated surveillance modulated by TH17 & Tregs
title_sort	influenza 2009 pandemic: cellular immunemediated surveillance modulated by th17 & tregs
description	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.
publisher	Biomedical Informatics
publishDate	2011
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3064851/
_version_	1611447112602484736

Influenza 2009 pandemic: Cellular immunemediated surveillance modulated by TH17 & Tregs

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