How HIV type 1 Clade B and C Tat Protein affects the regulation of Indoleamine-2,3-dioxygenase I was intensely interested on how HIV-1 Clads and Tat proteins appears to increase the level of neuro-pathogenic agents, such as indoleamine-2,3-dioxygenase (IDO) and kynurenine (KYN) which can cause HIV-1-associated dementia (HAD). This research paper is design to assess how HIV-1 clade tat protein affects the regulation of indoleamine-2,3-dioxygenase and how it may contribute to neurological disorder such as HIV/AIDS dementia. Also, the paper is design to analyze the role /effects and characteristic of HIV and HIV/Aids dementia on a minor scale. Research done by scientist would be used as a template to draw conclusive results. At
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It is transmitted by sexual contact, blood, and from mother to child. HIV-1 is the most recognized pathogenic strain of the virus. It is also related to virus found in chimpanzee and gorilla in West Africa. HIV-1 Tat protein is important to viral replication and infectivity. During acute infection, infected cells releases Tat by extracellular means and becomes engulfed by neighboring cells, where it activates viral replication thus increases virus infectivity. Vital brain cells known as neurons can be indirectly damaged by HIV. It infects macrophages and microglia-cells that nurture the brain, causing them to produce toxins that instruct neurons to kill themselves. Indoleamine 2,3-dioxygenase is a rate-limiting enzyme. It can degrade tryptophan through kynurenine pathway, which can cause halted growth of T cells. Indoleamine 2,3-dioxygenase has the ability to powerfully suppress immune activity, which contribute to the immune dysfunction observed in HIV-infected …show more content…
When HIV-1-clade C and HIV-1 clade B was compared, the latter produced an increase in the level of Indoleamine 2,3-dioxygenase activity and gene expression in astrocytes. The outcome of both Tat B and C on Kynurenine Manufacturing was quite significant. Samikkannu, Thangavel(2009) states that “the kynurenine levels induced by B Tat were significantly higher compared to Hiv 1 Tat-C . This suggests that the increased levels of kynurenine in the supernatant may be conditional on increased Indoleamine 2,3-dioxygenase gene expression.” The infection from HIV-1 Tat B over-invigorate Indoleamine 2,3-dioxygenase by glial cells. This caused the decrease of tryptophan while increasing the manufacturing of kynurenine to entice brain cell death. The research highlights how different HIV-1 clades can affect the yield of IDO and kynurenine in human astrocytes. The striking significant difference in results shows that HIV clade C Tat produced a very low level of kynurenine, however there was an absence of meaningful installment of IDO gene expression. According to Thomas SR, Salahifar H, Mashima R (2001), “in the study of astrocytes treated by Tat B, we observed a high degree of increased expression of the IDO gene, protein, IDO enzyme activity and kynurenine concentration simultaneously. Whereas astrocytes treated by Tat C demonstrated a slight increase only in IDO enzyme activity, while kynurenine concentration resulted
It is transmitted by sexual contact, blood, and from mother to child. HIV-1 is the most recognized pathogenic strain of the virus. It is also related to virus found in chimpanzee and gorilla in West Africa. HIV-1 Tat protein is important to viral replication and infectivity. During acute infection, infected cells releases Tat by extracellular means and becomes engulfed by neighboring cells, where it activates viral replication thus increases virus infectivity. Vital brain cells known as neurons can be indirectly damaged by HIV. It infects macrophages and microglia-cells that nurture the brain, causing them to produce toxins that instruct neurons to kill themselves. Indoleamine 2,3-dioxygenase is a rate-limiting enzyme. It can degrade tryptophan through kynurenine pathway, which can cause halted growth of T cells. Indoleamine 2,3-dioxygenase has the ability to powerfully suppress immune activity, which contribute to the immune dysfunction observed in HIV-infected …show more content…
When HIV-1-clade C and HIV-1 clade B was compared, the latter produced an increase in the level of Indoleamine 2,3-dioxygenase activity and gene expression in astrocytes. The outcome of both Tat B and C on Kynurenine Manufacturing was quite significant. Samikkannu, Thangavel(2009) states that “the kynurenine levels induced by B Tat were significantly higher compared to Hiv 1 Tat-C . This suggests that the increased levels of kynurenine in the supernatant may be conditional on increased Indoleamine 2,3-dioxygenase gene expression.” The infection from HIV-1 Tat B over-invigorate Indoleamine 2,3-dioxygenase by glial cells. This caused the decrease of tryptophan while increasing the manufacturing of kynurenine to entice brain cell death. The research highlights how different HIV-1 clades can affect the yield of IDO and kynurenine in human astrocytes. The striking significant difference in results shows that HIV clade C Tat produced a very low level of kynurenine, however there was an absence of meaningful installment of IDO gene expression. According to Thomas SR, Salahifar H, Mashima R (2001), “in the study of astrocytes treated by Tat B, we observed a high degree of increased expression of the IDO gene, protein, IDO enzyme activity and kynurenine concentration simultaneously. Whereas astrocytes treated by Tat C demonstrated a slight increase only in IDO enzyme activity, while kynurenine concentration resulted