Possible roles of oxidative stress, local circulatory failure and nutrition factors in the pathogenesis of hypervirulent influenza: Implications for therapy and global emergency preparedness

In discussions about emergency preparedness for a possible global pandemic of hypervirulent influenza, one factor is conspicuously absent when the matter is discussed in political fora, and in most of the papers published in medical journals, i.e. the possible role of nutrition factors in host vulnerability to the disease

Olav Albert Christophersen; Anna Haug

2006

Scholarcy highlights

  • In discussions about emergency preparedness for a possible global pandemic of hypervirulent influenza, one factor is conspicuously absent when the matter is discussed in political fora, and in most of the papers published in medical journals, i.e. the possible role of nutrition factors in host vulnerability to the disease
  • It must be expected that consequences of nutritional deficiency conditions that weaken the Th1-mediated immune response must be qualitatively similar in all viral infections including influenza, with a weakening of the Th1 response causing enhanced morbidity and – for the more dangerous infections – enhanced mortality
  • There is strong reason to expect that morbidity and mortality will be higher for any form of influenza in poorly nourished populations, with intakes of selenium and sulfur amino acids being perhaps the most critical factors, and B-group vitamins needed for the normal operation of the glutathione reductase and thioredoxin reductase systems, as well as several other micronutrients and conditionally essential nutrients needed for optimal function of the immune system
  • Diet-induced deficiency of folate and/or vitamin B12 is common in many poor countries, with the situation as regards vitamin B12 being especially alarming in parts of India
  • When nutrition factors are important for so many different aspects of the disease process, it means that there should be good possibilities of therapeutic intervention with a quadruple aim: optimizing antioxidant protection of the lungs and other organs that might be attacked by the virus; defending mitochondrial function and the local circulation in these organs; reducing oxidative activation of NF-kappaB in an effort to minimize the stimulating effect of NF-kappaB on the replication of the virus; optimizing the function of the immune system, with special emphasis on the function of NK cells and cytotoxic CD8+ cells

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