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AofA Science Summary: Inhibition of influenza infection by glutathione.

Science post image Free Radic Biol Med. 2003 Apr 1;34(7):928-36.

Inhibition of influenza infection by glutathione.

Cai JChen YSeth SFurukawa SCompans RWJones DP.

Source

Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA. jcai@learnlink.emory.edu

Abstract

Infection by RNA virus induces oxidative stress in host cells. Accumulating evidence suggests that cellular redox status plays an important role in regulating viral replication and infectivity. In this study, experiments were performed to determine whether the thiol antioxidant glutathione (GSH) blocked influenza viral infection in cultures of Madin-Darby canine kidney cells or human small airway epithelial cells. Protection against production of active virus particles was observed at a low (0.05-0.1) multiplicity of infection (MOI). GSH inhibited expression of viral matrix protein and inhibited virally induced caspase activation and Fas upregulation. In BALB/c mice, inclusion of GSH in the drinking water decreased viral titer in both lung and trachea homogenates 4 d after intranasal inoculation with a mouse-adapted influenza strain A/X-31. Together, the data suggest that the thiol antioxidant GSH has an anti-influenza activity in vitro and in vivo. Oxidative stress or other conditions that deplete GSH in the epithelium of the oral, nasal, and upper airway may, therefore, enhance susceptibility to influenza infection.

 

Comments

Karin

The glutathione-depleting drug Tylenol is added to many cold/flu over-the-counter formulations, isn't it a great idea then! (Sarcasm)

The recommendation of giving Tylenol to babies before and after their immunizations also makes great sense, especially for live virus vaccines, right! (Double-sarcasm)

Kelly

Oxidative stress from chronic inflammation will raise glutamate, reduce cysteine, reduce glutathione. Vicious cycle. This chronic state has the cell calling for more 1,25D to signal gene transcription to fight the fire of inflammation, whether injury, pathogens, or toxins. But the call never subsides, steroid 1,25D rises and rises (using up 25D), de-sensitizing the signal to transcribe over 1000 genes and disturbing other important cell receptors like ER (estrogen) which has an effect on 26% of our genome. We have 52 nuclear cell receptors at current count that orchestrate the signals for gene transcription. We need to understand how to keep them working. Current medicine paradigm is mostly immune suppressive drugs which we need desperately to review. Changing the chemical environment in the cell will alter function in an almost infinite number of pathways. Chronic inflammation will stop your ability to make the antimicrobial peptides to keep pathogens out. Once the pathogens are in, they will continue the chronic inflammation process. Vicious, vicious cycle. Over a lifetime, this is an inevitable, gradual process. But our canaries are teaching us that messing with mother nature can be heartbreaking. A toxic world lets in the pathogens way too early.

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