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Table 1 Low-cost, readily available drugs with immunomodulatory activities that could benefit patients with severe influenza

From: The dysfunctional host response to influenza A H7N9: a potential treatment option?

Drug class Proposed mechanism of protection for influenza Level of evidence
HMG CoA reductase inhibitors (statins); lipid-lowering agents with numerous anti-inflammatory and vasoprotective effects Alter prenylation pattern of enzymes and membranes: vaso-protection; lower TLR signaling; reduce oxidative stress; upregulate eNOS; upregulate AMPK and PGC-1 alpha; reduce NADPH oxidase activity Animal studies; numerous observational studies in pneumonia and one in human influenza; one randomized, controlled trial in human sepsis
Aspirin, a cyclooxygenase inhibitor, might potentiate statin effects Unknown, may shunt oxygenated lipid precursors to lipooxygenase pathway; might amplify statin actions Observational studies in patients with severe pneumonia
PPAR-gamma agonists (thiazolidinediones, glitazones); anti-diabetic treatments with effects on mitochondrial biogenesis Agonist for PGC-1 alpha that promotes mitochondrial function and biogenesis, might limit apoptosis Animal studies with influenza virus challenge models
PPAR-alpha agonists (fibrates); lipid-lowering agents with effects on mitochondrial biogenesis Promotes mitochondrial function, biogenesis Animal studies with influenza virus challenge models
Angiotension II inhibitors – ARB agents and ACE inhibitors Blocks angiotensin II ligation to AT-1, limiting superoxide generation by NADPH oxidase Human observational studies in pneumonia patients, no data on influenza patients thus far
AMPK agonists (metformin), anti-diabetic agents with immune-metabolic effects AMPK reduces oxidant stress and induces anti-apoptotic signals Preclinical studies, no data in influenza patients thus far
Resveratrol, a polyphenol nutritional supplement Stimulates sirtuin activity, activates PPAR alpha and PGC-1 alpha, protects against oxidant stress Improved survival in animal studies with influenza challenge models
  1. ACE, angiotensin-converting enzyme; AMPK, adenosine monophosphate protein kinase; ARB, angiotensin receptor blocker; AT-1, angiotensin II type 1 receptor; eNOS, endogenous endothelial nitric oxide synthase; HMG CoA, 3-hydroxy-3-methylglutaryl coenzyme A; NADPH, nicotinamide adenine dinucleotide phosphate hydrogen; PGC-1 alpha, peroxisome proliferator activated receptor gamma coactivator-1 alpha; PPAR, peroxisome proliferator activated receptor; TLR, toll like receptor.