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The Treatment of HIV-1, Research Paper Example
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The treatment of HIV-1 infections has been topic of concern for many researchers. One team of researchers has investigated the outcome of treatment of the elimination of latently infected cells in combination with antiretroviral therapy (cART) in HIV-1 infection patients. Researchers indicate that the viral replication of HIV occurs during treatment interruption and individuals must continue with cART in order to reduce HIV replication, which puts patients at risk for other diseases. However, with the elimination of latently infected cells in these patients, would decrease the need for treatment with cART. In this study, a single immunomodulatory protein was generated to help activate CD4 cells latently infection with HIV-1 and result in their lysis using a bispecific protein. In order to determine the response of T cells after exposure to HIV-1, the human CD4 and CD8 cell response was analyzed in presence and absence of HIV-1. The results of the study showed a nine fold increase in CD4 T cell response, which suggests this could help eliminate HIV-1 latent infected cells, as well as the reservoir of HIV.[1]
Per the National Institute of Health (NIH), a new protein called the VRC07-?CD3 has been developed. This protein helps destroy HIV infected resting immune cells and could facilitate towards a cure for individuals infected with HIV. The protein works by depleting the reservoir of resting HIV-infected immune cells. Research has shown positive results for the VRC07-?CD3 protein during laboratory investigations using human T-cells, as well as applying the protein to research monkeys carrying the simian version of HIV. The physical structure of the protein is composed of two ends. One of the ends activates T-cells through the binding to a surface molecule, referred to as the CD3 receptor. The other end binds an antibody called the VRC07, which binds to over 90 percent of HIV strains. The process by which VRC07-?CD3 destroys the HIV cells occurs through three specific steps. First, the protein binds to the CD3 receptor of the resting HIV T-helper cell, which activates the cell and produces HIV on the cell surface. Second, the HIV-binding end of the protein binds to the virus and the CD3-binding end binds to a killer T cell. The killer T cell in turn destroys the HIV infected cell. [2] The results of these studies suggest new approaches to the contribution of total eradication of HIV reservoirs in HIV infected individuals.
[1] Burke, B.P., Boyd, M.P., Impey, H., Breton, L.R., Bartlett, J.S. CCR5 as a Natural and Modulated Target for Inhibition of HIV. 2014. Viruses. 6(54-68). 9
[2] Pegu, A., Asokan, M, Wul, L., Wang, K, Hatayel, J. Casazzal, JP., Guo, X, Shi W, Georgiev I, Zhou, T, O’Deil S, Tood, JP, Kwong, PD, Raol, SS, Yang, Z, Koup RA, Masolal JR, Nabe GJ. Activation and lysis of human CD4 cells latently infected with HIV-1. Aug 2015. Nature Communications. Pgs 1-9.
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