Abstract |
A main feature of HIV infection is the expression of several proinflammatory cytokines. Proinflammatory cytokines expressed as soluble factors or membrane-bound molecules regulate both HIV replication and T cell apoptosis. Proinflammatory cytokines have key roles in the HIV lifecycle, especially at the level of transcription, favouring the ability of HIV to establish latent reservoirs. In addition, proinflammatory cytokines are involved in both CD4+ T cell and CD8+ T cell apoptosis, resulting in immune suppression. Moreover, several HIV proteins such as Nef, Tat, and Vpr hijack proinflammatory cytokine signaling, further underlining the potential importance of inflammation in HIV pathogenesis. In vivo chronic inflammatory conditions have been correlated to increased levels of viremia and accelerated disease progression. This article raises the possibility that inflammation plays a crucial role in both immune suppression and the formation of viral reservoirs during HIV infection. Understanding the role of inflammation in HIV infection could lead to new therapeutic strategies that could ultimately enhance immune restoration and limit the formation of viral reservoirs in HIV-infected patients.
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Authors | Anne Zelie Decrion, Isabelle Dichamp, Audrey Varin, Georges Herbein |
Journal | Current HIV research
(Curr HIV Res)
Vol. 3
Issue 3
Pg. 243-59
(Jul 2005)
ISSN: 1570-162X [Print] Netherlands |
PMID | 16022656
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
- Cytokines
- Gene Products, nef
- Gene Products, tat
- Gene Products, vpr
- Inflammation Mediators
- nef Gene Products, Human Immunodeficiency Virus
- tat Gene Products, Human Immunodeficiency Virus
- vpr Gene Products, Human Immunodeficiency Virus
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Topics |
- Apoptosis
- CD4-Positive T-Lymphocytes
(immunology, pathology)
- CD8-Positive T-Lymphocytes
(immunology, pathology)
- Cytokines
(biosynthesis)
- Gene Products, nef
(immunology)
- Gene Products, tat
(immunology)
- Gene Products, vpr
(immunology)
- HIV Infections
(etiology, immunology, pathology, virology)
- HIV-1
(immunology, physiology)
- Humans
- Inflammation
(etiology, immunology, pathology)
- Inflammation Mediators
(metabolism)
- Models, Immunological
- Signal Transduction
- Virus Replication
(immunology)
- nef Gene Products, Human Immunodeficiency Virus
- tat Gene Products, Human Immunodeficiency Virus
- vpr Gene Products, Human Immunodeficiency Virus
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