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    T Cell Activation and Associated Susceptibility to HIV-1 Infection in vitro Increased Following Acute Exercise in Human Subjects

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    Dissertation (PDF) (1.888Mb)
    Author
    Holbrook, Alexander Keenan
    Date
    2019-05-03

    Degree
    MS (Master of Science), Medical Microbiology and Immunology
    Copyright: Thesis/Dissertation © Alexander Holbrook, 2019

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    Abstract

    Abstract
    Conventional belief suggests exercise generates a transient immunosuppressive effect in humans. Recent research suggests it may be time to rethink this hypothesis, as acute bouts of exercise have been shown to increase both lymphocyte activation and proliferation. The purpose of this study was to quantify exercise-induced changes in the activation state of CD4+ T cells by analyzing surface protein expression and the replication of a medically relevant viral model. This was accomplished by measuring the expression of CD4+ T cell activation markers (CD69, CD25, and HLA-DR) in both non-stimulated and stimulated cells (costimulation through CD3 and CD28) following an acute bout of resistance training in previously untrained individuals. Exercised-induced effects on intracellular activation was further evaluated via in vitro infection with type 1 human immunodeficiency virus (HIV-1). The results showed that non-stimulated CD4+ T cells exhibited elevated CD25 expression at 24 hours post-exercise. Increased replication of HIV-1 in the post-exercise cells was also observed 3 days after infection. Combined, these results suggest that acute exercise increases the activation state of CD4+ T cells. Given these findings, we further investigated whether the changes induced by an acute bout of exercise would increase the efficiency of latent infection in quiescent CD4+ T cells. The results however the establishment of HIV-1 latency did not increase upon reactivation post exercise. This work strengthens the evidence for exercise-induced T cell activation and demonstrates the use of medically relevant pathogens as indirect measures of intracellular activation states.
    URI
    http://hdl.handle.net/10504/122628
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