Infectious Diseases & HIV/AIDS

It has long been thought that the nutritional status can influence an individual's susceptibility to infection as well as the severity of the infection. In support of this contention, numerous investigations have found that diets deficient in one or more nutrients could exacerbate an infection. The basis for this increased susceptibility and virulence was originally thought to be a reduced level of immune function secondary to the underlying nutritional deficiency. However, in a very elegant series of investigations using both an animal model and humans, Beck and coworkers found that an antioxidant deficiency not only decreased specific immune functions, but also led to specific mutational changes in the viral genome such that a normally avirulent virus became virulent. It was also shown that once these mutations occurred, even mice with normal nutrition developed disease when exposed to the mutated virus. In the human population studied, patients who developed clinical sequelae from viral exposure had lower serum levels of several nutrients, including vitamin B2, selenium, carotenes and lycopene, than a control, non-infected group. Furthermore, investigations of influenza virus have found that oxidative stress influenced both the infectivity as well as the severity of the infection. One study found that infected mice supplemented with vitamin E had reduced viral titers, less appetite loss, and one-third less weight loss compared with infected, non-supplemented mice.

 

In addition to acute infections, chronic viral infection has been associated with increased oxidative stress and subsequent increased probability of progression to viral-associated carcinoma. Yu et al. followed over 7000 chronic hepatitis C men for an average of 5.3 years. Those patients who progressed to hepatocellular carcinoma (HCC) had lower mean plasma selenium levels and decreased levels of carotenoids than patients who did not develop HCC. Subsequently, Emerit et al. found that 19 of 20 patients chronically infected with hepatits C virus had higher than normal levels of lipid peroxidation products and other oxidants that had chromosome-damaging properties. Finally, Ho et al. examined nutrition as a potential, independent risk factor in the progression of genital human papillomavirus (HPV) to cervical intraepithelial neoplasia (CIN). In a case control study they found an inverse correlation between plasma alpha-tocopherol levels and the risk of CIN.

 

Human immunodeficiency viral (HIV) infection represents another example where the progression of HIV infection to AIDS appears to be influenced by nutritional factors, especially by antioxidants and vitamin B12. Insufficient intake, malabsorption, diarrhea, impaired storage, altered metabolism and increased usage can all contribute to the nutritional deficiencies observed in HIV infected individuals. Deficiencies of vitamins A, E, B6, B12 and C, carotenoids, selenium, glutathione, zinc and total thiol (cysteine) levels are prevalent in HIV infected populations. It is now believed by many investigators that the major pathologic feature of HIV infection is the generation of oxidative stress, secondary to overproduction of reactive oxygen species and depletion of antioxidants. This process in turn leads to apoptosis (programmed cell death) and consequent depletion of CD4 cells. Combinations of the nutrient deficiencies listed above are believed to contribute to the generation of the free radical overload that promotes the apoptosis of CD4 T lymphocytes. In addition to antioxidants, deficiencies of vitamin B12 and glutamine appear to be especially relevant to HIV disease progression. In a non-concurrent prospective cohort study of 310 HIV seropositive subjects, Tang et al. found that those participants with low serum B12 had significantly shorter AIDS-free time than those with adequate B12 levels. And, HIV infection appears to induce glutamine deficiency, possibly secondary to the rapid turnover of immune cells that occurs in most stages of the infection.

 

SpectraCell's antioxidant panel, the Spectrox + glutathione tests, can be used to estimate antioxidant defenses in either acute or chronic infections, especially hepatitis C virus and HIV. FIA™ tests for functional deficiencies of B vitamins, zinc, magnesium, and glutamine can also be valuable in designing individual combinations of supplements that may help your patients avoid, delay or slow the progression of viral disease.

 

REFERENCES

1. Dietary oxidative stress and the potentiation of viral infection. Beck MA and Levander OA. Annu Rev Nutr. 1998;18:93-116.
2. The role of oxidative stress in viral infections. Beck MA et al. Ann NY Acad Sci. 2000;917:906-912.
3. Host nutrition status and its effect on a viral pathogen. Beck MA and Levander OA. J Infect Dis. 2000;182 Suppl 1:S93-S96.
4. Nutritionally induced oxidative stress: effect on viral disease. Beck MA. Am J Clin Nutr. 2000;71(6Suppl):1676S-1681S.
5. Alterations in antioxidant defenses in lung and liver of mice infected with influenza A virus. Mennet T et al. J Gen Virol. 1992;73:39-46.
6. Effect of long-term dietary antioxidant supplementation on influenza virus infection. Han SN et al. J Gerontol A Biol Sci Med Sci. 2000;55:B496-503. (CHECK THIS)
7. Plasma selenium levels and risk of hepatocellular carcinoma among men with chronic hepatitis virus infection. Yu MW et al. Am J Epidemiol. 1999;150:367-374.
8. Clastogenic factors as biomarkers of oxidative stress in chronic hepatitis C. Emerit C et al. Digestion 2000;62:200-207.
9. Viral characteristics of human papillomavirus infection and antioxidant levels as risk factors for cervical dysplasia. Ho GY et al. Int. J Cancer 1998;78:594-599.
10. Nutrients and HIV: part one – beta carotene and selenium. Patrick L. Altern Med Rev. 1999;4:403-413.
11. Nutrients and HIV: part two – vitamins A and E, zinc, B-vitamins, and magnesium. Patrick L. Altern Med Rev. 2000;5:39-51.
12. Nutrients and HIV: part three – N-acetylcysteine, alpha-lipoic acid, L-glutamine, and L-carnitine. Patrick L. Altern Med Rev. 2000;5:290-305.
13. The role of oxidative stress in HIV disease. Pace GW and Leaf CD. Free Radic Biol Med. 1995;19:523-528.
14. Oxidative stress as a mediator of apoptosis. Buttke TM and Sandstrom PA. Immunol Today 1994;15:7-10.
15. HIV-induced cysteine deficiency and T-cell dysfunction – a rationale for treatment with N-acetylcysteine. Dröge W et al. Immunol Today. 1992;13:211-214.
16. Low serum vitamin B-12 concentrations are associated with faster human immunodeficiency virus type 1 (HIV-1) disease progression. Tang AM et al. J Nutr. 1997;127:345-351.
17. Glutamine deficiency as a cause of human immunodeficiency virus wasting. Shabert JK and Wilmore DW. Med Hypotheses. 1996;46:252-256.
18. Glutamine-antioxidant supplementation increases body cell mass in AIDS patients with weight loss: a randomized, double-blind controlled trial. Shabert JK et al. Nutrition. 1999;15:860-864.

 

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