tetano
Editor, Senior Moderator
Virology. 2013 Jul 19. pii: S0042-6822(13)00396-6. doi: 10.1016/j.virol.2013.06.026. [Epub ahead of print]
Glycolytic control of vacuolar-type ATPase activity: A mechanism to regulate influenza viral infection.
Kohio HP, Adamson AL.
Source
Department of Biology, University of North Carolina at Greensboro, Greensboro, NC 27402, USA.
Abstract
As new influenza virus strains emerge, finding new mechanisms to control infection is imperative. In this study, we found that we could control influenza infection of mammalian cells by altering the level of glucose given to cells. Higher glucose concentrations induced a dose-specific increase in influenza infection. Linking influenza virus infection with glycolysis, we found that viral replication was significantly reduced after cells were treated with glycolytic inhibitors. Addition of extracellular ATP after glycolytic inhibition restored influenza infection. We also determined that higher levels of glucose promoted the assembly of the vacuolar-type ATPase within cells, and increased vacuolar-type ATPase proton-transport activity. The increase of viral infection via high glucose levels could be reversed by inhibition of the proton pump, linking glucose metabolism, vacuolar-type ATPase activity, and influenza viral infection. Taken together, we propose that altering glucose metabolism may be a potential new approach to inhibit influenza viral infection.
Copyright ? 2013 Elsevier Inc. All rights reserved.
KEYWORDS:
Glucose, Glycolysis, Influenza, V-ATPase
PMID:
23876457
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23876457
Glycolytic control of vacuolar-type ATPase activity: A mechanism to regulate influenza viral infection.
Kohio HP, Adamson AL.
Source
Department of Biology, University of North Carolina at Greensboro, Greensboro, NC 27402, USA.
Abstract
As new influenza virus strains emerge, finding new mechanisms to control infection is imperative. In this study, we found that we could control influenza infection of mammalian cells by altering the level of glucose given to cells. Higher glucose concentrations induced a dose-specific increase in influenza infection. Linking influenza virus infection with glycolysis, we found that viral replication was significantly reduced after cells were treated with glycolytic inhibitors. Addition of extracellular ATP after glycolytic inhibition restored influenza infection. We also determined that higher levels of glucose promoted the assembly of the vacuolar-type ATPase within cells, and increased vacuolar-type ATPase proton-transport activity. The increase of viral infection via high glucose levels could be reversed by inhibition of the proton pump, linking glucose metabolism, vacuolar-type ATPase activity, and influenza viral infection. Taken together, we propose that altering glucose metabolism may be a potential new approach to inhibit influenza viral infection.
Copyright ? 2013 Elsevier Inc. All rights reserved.
KEYWORDS:
Glucose, Glycolysis, Influenza, V-ATPase
PMID:
23876457
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23876457