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The Many Faces of Immune Activation in HIV-1 Infection: A Multifactorial Interconnection

Persistent activation is observed in numerous components of both the innate and adaptative immune system, including cells (e.g., activated phenotypes of macrophages and dendritic cells), cytokines and chemokines [tumor necrosis factor, interleukin (IL)-1, IL-6, IL-8, IL-15, and IL-10], acute phase proteins (serum amyloid A, C-reactive protein), elements of the coagulation cascade (D-dimers, tissue factor), elements of fibrosis (matrix metalloproteinase activation, collagen deposition), and microbial sensors (lipopolysaccharide binding protein, soluble CD14). Increased turnover and exhaustion of T cells and turnover of B cells are observed with an altered phenotypic profile and hypergammaglobulinemia . Moreover, high levels of systemic immune activation and inflammation not only promote viral replication and CD4+ T-cell apoptosis, but they may also lead to a more rapid decline of immune function and competence, which have been associated with aging

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