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Immunol Lett. 2014 Oct;161(2):184-8. doi: 10.1016/j.imlet.2014.01.008. Epub 2014 Jan 30.

Persistent inflammation in HIV infection: established concepts, new perspectives.

Author information

1
Department of Surgery, Medicine, Dentistry and Morphological Sciences, University of Modena and Reggio Emilia, Modena, Italy.
2
Department of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy.
3
Department of Surgery, Medicine, Dentistry and Morphological Sciences, University of Modena and Reggio Emilia, Modena, Italy; Infectious Diseases Clinics, Azienda Ospedaliero-Universitaria Policlinico di Modena, Modena, Italy.
4
Department of Surgery, Medicine, Dentistry and Morphological Sciences, University of Modena and Reggio Emilia, Modena, Italy. Electronic address: andrea.cossarizza@unimore.it.

Abstract

Immune activation is now considered a main driving force for the progressive immune failure in HIV infection. During the early phases of infection, a rapid depletion of gastrointestinal CD4+ T cells occurs that is followed by a deterioration of the gut epithelium and by the subsequent translocation of microbial products into the blood. Activation of innate immunity results in massive production of proinflammatory cytokines, which can trigger activation induced cell death phenomena among T lymphocytes. Moreover, persistent antigenic stimulation and inflammatory status causes immune exhaustion. The chronic immune activation also damages lymphoid tissue architecture, so contributing to the impairment of immune reconstitution. Recently, new mechanisms were identified, so opening new perspective on the innate immune sensing in HIV-1 infection. Cell death is followed by the release of molecules containing "damage-associated molecular patterns", that trigger a potent innate immune response through the engagement of Toll-like receptors. Then, also different types of HIV-related nucleic acids can act as potent stimulators of innate immunity. All these events contribute to the loss of T cell homeostatic regulation and to the failure of adaptive immunity.

KEYWORDS:

AIDS, CD4; HIV; Immune activation; Inflammation

PMID:
24487059
DOI:
10.1016/j.imlet.2014.01.008
[Indexed for MEDLINE]

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