HIV an infection is a global disease that disproportionately burdens populations with nutritional vulnerabilities. with increased syncytia formation and possibly prevention of apoptosis of those infected cells and therefore there was concern that selenium supplementation might lead to increased dissemination of the virus in the early stages of infection.4 5 Genetic studies of cellular immunity and of HIV’s genome revealed an interplay between selenium and genes important for propagation of the virus. Studies of T cells looking at the genes that encode CD4 CD8 and human leukocyte antigen DR 33 (HLA DR 33) were found to have open reading frames with multiples of UGA codons similar to those that encoded selenoproteins. These open reading frames also contained potential stem loop structures that could interact with selenocysteine residues. This was thought to be a highly unlikely coincidence and suggested that the interaction between selenium and HIV disease might be more complex than was previously understood. It was further proposed that selenoproteins might lie within the viral genome for some purpose.16 Two years later this hypothesis was verified by finding frameshift sites and RNA pseudoknots that would lead to selenoprotein synthesis when the encoding module for the selenoprotein overlapped another functioning gene. At that time similar structures were found in a wide range of other viruses suggesting selenium has a role to play in the virulence of multiple pathogens.17 A separate study found structures that encode glutathione peroxidase in a molluscum contagiosum virus and suggested that such structures might be found commonly in other viruses.18 Within a short time the hypothesis that HIV might encode selenoproteins was investigated and using a computer model it was discovered that the coding sequence in question was homologous to human glutathione peroxidase. When this gene was cloned and transfected into canine kidney cells it increased the output of glutathione peroxidase by 21 to 43% and in transfected MCFV7 cells by 100%.19 Within the field many once again postulated that selenium might be important to the needs of HIV itself or the virus’ interaction with the cell’s oxidative machinery when integrating into the host genome. Later advances in virology and immunology brought a T-cell model that could be used to study increases and decreases in oxidative signaling through an immortalized T-cell line that had been given a selenium dependent glutathione peroxidase construct via a retroviral vector.20 The same year as this result another experiment showed that selenium was important in the regulation of NFκB which is important in mitigating the effect of HIV pathogenesis through its effects in upregulating glutathione peroxidase.21 Following this it was discovered SMAX1 that selenium supplementation will decrease the replication of HIV when the virus is exposed to TNF-α confirming selenium’s role in up regulating other antioxidant enzymes.22 Researchers then found that the levels of normal selenoproteins that are expressed in T-cells including thiodoxin reductase glutathione peroxidase Refametinib and phospholipids hydroperoxide glutathione peroxidase are increased in the presence of Refametinib selenium but diminished when the T cell Refametinib is infected with HIV.22 23 low molecular mass compounds containing selenium are produced Instead.23 Therefore in lots of papers it turned out demonstrated that HIV benefited through the disruption of normal selenoprotein synthesis and from disrupting the functions of normal cellular oxidative activity. The query of whether HIV’s replicative equipment incapacitated the oxidative machinery of the T cell intentionally or unintentionally remained an open one but many researchers began to think it was intentional. Selenium appears to play a role as an immunomodulator as well. exposure of chronically infected T-lymphocyte and monocytic cell lines to selenium prior to exposure to TNFα resulted in decreased induction of HIV-1 replication. Interestingly there was a similar effect for acutely infected monocytic cell lines but not for T-cell lines.22 Selenium has also been shown to have a beneficial influence on creation of both interleukin 2 (IL-2) and its own receptor expression resulting in era of cytotoxic T lymphocytes and organic killer cells.24 25 It really is inversely correlated levels also.