Abstract
Infection of T cells by the Human Immunodeficiency Virus (HIV) renders the body susceptible to attack by opportunistic infections as these cells of the immune system are not only killed by the virus, but are also rendered defective in their function (1,2,3,4). It is well documented that T cell defects associated with HIV infection in AIDS patients include reduced production of the lymphokine, IL-2, and an inability to mobilize Ca++ following mitogenic or antigenic stimulation. T cell dysfunction has also been attributed to downmodulation of CD3 and CD4, possibly as a result in their uncoupling (5,6,7). Since many of these events that lead to T cell activation are under some of the same controls as events involved in the activation of HIV (8–9), a T cell model system to study physiologic influences on HIV expression and the effects of the virus on the cell’s activation signals would be of great value.
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© 1991 Plenum Press, New York
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Perez, V.L., Folks, T.M. (1991). A T Cell Clone Which Reflects the Functional Defects Observed in the T Cells of AIDS Patients. In: Kumar, A. (eds) Advances in Molecular Biology and Targeted Treatment for AIDS. GWUMC Department of Biochemistry Annual Spring Symposia. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5928-9_23
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DOI: https://doi.org/10.1007/978-1-4684-5928-9_23
Publisher Name: Springer, Boston, MA
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