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Asthma and influenza virus infection:focusing on cell death and stress pathways in influenza virus replication

tetano

Editor, Senior Moderator
Iran J Allergy Asthma Immunol. 2013 Mar;12(1):1-17. doi: 012.01/ijaai.117.
Asthma and influenza virus infection:focusing on cell death and stress pathways in influenza virus replication.
Yeganeh B, Rezaei Moghadam A, Tran AT, Rahim MN, Ande SR, Hashemi M, Coombs KM, Ghavami S.
Source

Department of Physiology, University of Manitoba, Winnipeg, Canada. Department of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg, Canada. saeid.ghavami@gmail.com, and kcoombs@cc.umanitoba.ca.
Abstract

Asthma is one of the fastest growing syndromes in many countries and is adding a huge cost to the health care system. Increasing reports have linked airway infectious diseases to asthma. Influenza is one of the most serious airway infectious diseases and in recent years there have been some serious influenza virus pandemics which caused increased fatality in numerous different populations. Diverse host response pathways during virus infection have been identified, including different cell death and survival pathways. These pathways include 1) programmed cell death I (apoptosis), 2) programmed cell death II (autophagy), and 3) endoplasmic reticulum stress with subsequent unfolded protein response (UPR). There has been extensive research on the regulatory roles of these pathways during the influenza virus life cycle. These studies address the benefits of enhancing or inhibiting these pathways on viral replication. Here we review the most recent and significant knowledge in this area for possible benefits to clinicians and basic scientist researchers in different areas of the respiratory and virology sciences.

PMID:
23454774
[PubMed - in process]

http://www.ncbi.nlm.nih.gov/pubmed/23454774
 
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