The emergence of new infectious diseases and existing diseases with new pathogenic properties is a growing global public health problem. AIDS and SARS are two examples. What factors contribute to the rapid evolution of viruses? Climate changes, agricultural practices, rainforest clearing, and air travel have been proposed. Nutritional status of the host has generally not been considered an important contributing factor to the emergence of infectious disease. However, it is clear that host nutritional status can influence not only the host response to the pathogen, but also can influence the viral genome (Beck et al, 2004).
Selenium (Se) has a direct effect against RNA viruses like influenza, measles, polio, hepatitis B & C, and HIV. In a Se-deficient host, normally harmless viruses can become virulent. For example, when Se-deficient mice are inoculated with benign Coxsackie B3 virus, the virus mutates into a virulent form that causes myocarditis similar to that seen in Keshan disease (Beck et al, 1995, 1998, 2003) and mortality increases significantly if the virus is co-administered with mercury, a Se antagonist (South et al, 2001).
Se appears to be a particularly important nutrient for people with HIV, and it has been suggested that Se deficiency, due to widespread low soil levels, is a major reason for the much faster spread of AIDS in Sub-Saharan Africa than in North America (Foster, 2003).
http://pathmicro.med.sc.edu/lecture/hiv7.htm
Se strongly inhibits HIV replication in vitro, inhibits viral cytotoxic effects and the reactivation of HIV-1 by hydrogen peroxide, and inhibits necrosis factor kappa alpha and beta, which are important cellular activators of HIV-1 (Look et al, 1997; Sappey et al, 1994). Moreover, Se deficiency is a significant predictor of HIV-related mortality (Baum & Shor-Posner, 1998; Campa et al, 1999) and viral load (Baeten et al, 2001). It was found that Se-deficient HIV patients are nearly 20 times more likely to die from HIV-related causes than those with adequate levels (Baum et al, 1997). The decline in blood Se levels occurs even in the early stages of the disease and is thus unlikely to be due to malnutrition or malabsorption (Look et al, 1997). Moreover, a study of HIV-1-seropositive drug users found low Se level to be a significant risk factor for developing mycobacterial disease, notably tuberculosis (Shor-Posner et al. 2002). Selenoproteins encoded by HIV, hepatitis C virus (HCV) and the Ebola virus (which causes acute haemorrhage) have been discovered that consume the host’s Se supply, thus reducing immune response (Taylor & Nadimpalli, 1999; Zhang et al, 1999; Taylor et al, 2000; Zhao et al. 2000).
HIV/AIDS sufferers tend to be deficient in the four major nutrients associated with the selenoenzyme, glutathione peroxidase. Professor Harold Foster from Canada argues that HIV causes AIDS by creating deficiencies in these key nutrients: Se and the amino acids tryptophan, cysteine and glutamine. He promotes his “Selenium CD4 T-cell tailspin hypothesis”, that the fall in Se and the key amino acids causes a reduction in CD4 cells (important immune cells), which in turn causes a further decline in Se. Opportunistic infections then take over (Foster, 2004). A trial is currently being conducted in Africa to test Foster’s nutritional HIV/AIDS intervention [www.hdfoster.com]
There is ample evidence for the need for a nutritional/antioxidant approach to control hepatitis C [link to “Selenium and hepatitis C: a treatment role”].
Given the high global incidences of HIV, hepatitis B and C, and other RNA viruses, including measles and influenza, the public health implications of the above findings are enormous.
Influenza
Every year, global infection with influenza virus results in significant illness and death. In the US alone, over 20,000 deaths occur annually as a consequence of infection with influenza virus and its complications. Each year new strains evolve in China (where there are ample opportunities for transmission of zoonoses from poultry and pigs to humans in the vast Se-deficient belt), and make their way to Australia.
Se-deficient mice infected with a mild strain of influenza virus develop much more severe and prolonged lung inflammation than infected Se-adequate mice. Passage through the Se-deficient animals caused mutations in the virus, which included 29 nucleotide alterations in the gene for the M1 matrix protein, a viral protein previously thought to be relatively stable (Beck, 2001).
Baeten JM, Mostad SB, Hughes MP, Overbaugh J, Bankson DD, Mandaliya K, Ndinya-Achola JO, Bwayo JJ, Kreiss JK 2001. Selenium deficiency is associated with shedding of HIV-1-infected cells in the female genital tract. J Acqu Imm Defic Syndr 26(4): 360-364.
Baum MK, Shor-Posner G, Lai S 1997. High risk of HIV-related mortality is associated with selenium deficiency. J Acqu Imm Defic Syndr 15: 370-374.
Baum MK, Shor-Posner G 1998. Micronutrient status in relationship to mortality in HIV-1 disease. Nutr Rev 56(1): S135-S139.
Beck MA, Shi Q, Morris VC, Levander OA 1995. Rapid genomic evolution of a non-virulent Coxsackievirus B3 in selenium-deficient mice results in selection of identical virulent isolates. Nature Medicine 1: 433-436.
Beck MA, Esworthy RS, Ho YS, Chu FF 1998. Glutathione peroxidase protects mice from viral-induced myocarditis. Fed Am Soc Exp Biol J 12: 1143-1149.
Campa A, Shor-Posner G, Indacochea F 1999. Mortality risk in selenium-deficient HIV-positive children. J Acqu Imm Defic Syndr 20: 508-513.
Look MP, Rockstroh JK, Rao GS, Kreuzer KA, Spengler U, Sauerbruch T 1997. Serum selenium versus lymphocyte subsets and markers of disease progression and inflammatory response in human immunodeficiency virus-infection Biol Trace Elem Res 56: 31-41.
Sappey C, Legrand-Poels S, Best-Belpomme M, Favier A, Rentier B, Piette J 1994. Stimulation of glutathione peroxidase activity decreases HIV type 1 activation after oxidative stress. AIDS Res Human Retrovir 10: 1451-1461.
Shor-Posner G, Miguez MJ, Pineda LM, Rodriguez A, Ruiz P, Castillo G, Burbano X, Lecusay R, Baum M 2002. Impact of selenium status on the pathogenesis of mycobacterial disease in HIV-1-infected drug users during the era of highly active antiretroviral therapy. J Acqu Imm Defic Syndr 29(2): 169-173.
Taylor EW, Nadimpalli RG 1999. Chemoprotective mechanisms of selenium in cancer and AIDS: evidence for the involvement of novel selenoprotein genes. Info Onkologi 2: 7-11.
Yu SY, Zhu YJ, Li WG 1997. Protective role of selenium against hepatitis b virus and primary liver cancer in Qidong. Biol Trace Elem Res 56: 117-124.
Yu MW, Horng IS, Chiang YC, Liaw YF, Chen CJ 1999. Plasma selenium levels and the risk of hepatocellular carcinoma among men with chronic hepatitis virus infection. Am J Epidemiol 150: 367-374.
Zhao L, Cox AG, Ruzicka JA, Bhat AA, Zang W, Taylor EW 2000. Molecular modelling and in vitro activity of an HIV-1 encoded glutathione peroxidase. Proc Nat Acad Sci U S A 97: 6356-6361.
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