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Microbial products, especially bacterial lipopolysaccharide (LPS), contribute to immune activation. Increasing evidence indicates that T lymphocyte homeostasis disruptions are associated with immune activation. However, the mechanism by which LPS affects disruption of immune response is still not fully understood. Chronically SHIV<jats:sub>B\u2019WHU<\/jats:sub>-infected Chinese rhesus macaques received 50\u2009<jats:italic>\u03bc<\/jats:italic>g\/kg body weight LPS in this study. LPS administration affected the virus\/host equilibrium by elevating the levels of viral replication and activating T lymphocytes. LPS induced upregulation of CD8<jats:sup>+<\/jats:sup>na\u00efve T cells and downregulated the number of CD4<jats:sup>+<\/jats:sup>and CD8<jats:sup>+<\/jats:sup>T effector memory cells. The downregulated effector memory cells are associated with a lower frequency of monofunctional and polyfunctional cells, and an upregulated programmed cell death-1 (PD-1) expression on CD4<jats:sup>+<\/jats:sup>and CD8<jats:sup>+<\/jats:sup>T cells was observed in monkeys after LPS stimulation. 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