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Chronic Systemic Immune Activation in HIV-1 Infection

Call for Papers

All stages of HIV-1 infection are characterized by immune dysregulation. On the one hand, there is immunodepletion caused by the continuous loss of CD4+ cells and eventual exhaustion of lymphopoiesis. On the other hand, HIV-1 infection is also characterized by immune activation, mediated by the secretion of potent proinflammatory cytokines and chemokines. The causes of immune activation in the context of HIV-1 infection are poorly understood; however, the sustained immune activation that is observed during chronically replicating HIV infection has been associated with disease progression, immunosenescence, and adverse outcomes. Even in patients on long-term successful antiretroviral treatment (ART) who maintain undetectable viral loads and normal CD4 counts, low levels of immune activation can still be detected and are the best predictor of non-AIDS events. Knowledge and understanding of this immune activation and inflammation might provide additional measures which will help improve patient outcome.

We invite investigators to contribute original research articles as well as review articles that will stimulate the continuing efforts and help define the role of immune activation as well as measures to reduce proinflammatory and immune activation markers in HIV-infected individuals.

Potential topics include but are not limited to the following:

  • Immunological consequences of chronic systemic immune activation
  • Impact of chronic systemic immune activation on AIDS and non-AIDS events and accelerated aging
  • Role of HIV coinfection in chronic systemic immune activation
  • Strategies to reduce chronic systemic immune activation in HIV-infected individuals

Authors can submit their manuscripts through the Manuscript Tracking System at https://mts.hindawi.com/submit/journals/mi/csia/.

Submission DeadlineFriday, 13 July 2018
Publication DateNovember 2018

Papers are published upon acceptance, regardless of the Special Issue publication date.

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