Nutritional Processes in HIV/AIDS

So, if you live in an area of the world where there are high levels of selenium in the soil and diet, why are you protected against HIV infection?

By looking at the biochemical roles of this essential mineral in metabolic processes in the body, we can uncover the answers. One particular role it plays, which protects the body against pathogens like HIV, is in an enzyme called glutathione peroxidase which blocks HIV from replicating and infecting individuals.1

Glutathione peroxidase is called a selenoenzyme because it is made up of selenium, and the amino acids cysteine, tryptophan and glutamine.

Cleverly, HIV makes a homologue (copy) of glutathione peroxidase2 as it replicates.  Therefore, the virus competes in HIV-positive individuals for the very nutrients that are required to make the enzyme which protects them from the virus.   As the viral load increases, the levels of selenium, cysteine, glutamine and tryptophan decrease and so does the amount of glutathione peroxidase in the body, making it easier for the virus to replicate. 3,4,5,6,7

Dr. Harold Foster, who discovered this process, calls this positive feedback system the ‘selenium-CD4 T cell tailspin’ which becomes more and more dangerous over time. Eventually, after a period of time, the length of which depends on the diet being eaten, this depletion process of the four key nutrients causes severe nutritional deficiency symptoms progressing the severity of the disease.

These nutrient deficiencies are a major component of a weakened immune system, muscle wasting, malabsorption, poor digestion, dermatitis, diarrhea and many other health issues.  As a result, death is often caused by opportunistic infection, cancers, or organ failure.

Current antiretroviral therapy targets the virus, inhibiting replication and decreasing viral load. For optimal recovery of the immune system and to restore the distinctive nutritional deficiencies of PLWHA, the provision of a carefully designed micronutrient supplement is recommended to replenish nutrient deficiencies which cannot be satisfied by changes in diet alone.

Sources:

  1. Taylor, E.W. Selenium and viral diseases: Facts and hypotheses. JOM, 1997: 12(4), 227-239.
  2. Taylor EW, BHat A, Nadimpalli RG, Zhang W, Kececioglu J. HIV-1 encodes a sequence of overlapping env. gp41 with highly significant similarity to selenium dependent glutathione peroxidases. J AIDS Hum Retrovirol 1997; 15(5):393-4.
  3. Moriorino M, Aumann KD, Brigelius-Flohe R et al: Probing the presumed catalytic triad of a selenium-containing peroxidise by mutational analysis. Z. Ernahrungswiss, 1998; 37(Suppl. 1):118-121.
  4. Aumann KD, Bedorf N, Brigelius-Flohe R, Schomburg D, Flohe L. Glutathione peroxidase revisited – simulation of the catalytic cycle by computer-assisted molecular modeling. Biomed Environ Sci 1997; 10(2-3):136-55.
  5. Moriorino M, Aumann KD, Brigelius-Flohe R, Doria D, van den Heuvel J, McCarthy J, et al. Probing the presumed catalytic triad of selenium-containing peroxidises by mutational analysis of phospholipid hydroperoxidase glutathione peroxidise (PHGPx). Biol Chem Hoppe Seyler 1995; 376(11):650-1.
  6. Foster, H.D. (2000). AIDS and the “selenium-CD4 T cell tailspin”: The geography of a pandemic. Townsend Letters for Doctors and Patients, 209, 94-99.
  7. Ho, W.Z., and Douglas, S.D. Glutathione and N-acetyl-cysteine suppression of human immunodeficiency virus replication in human monocyte/macrophages in vitro. AIDS Research and Human Retroviruses, 1992; 8(7), 1249-1253.