Oxidative stress in human immunodeficiency virus infection

@article{Israel1997OxidativeSI,
  title={Oxidative stress in human immunodeficiency virus infection},
  author={Nicole Israël and Marie Anne Gougerot-Pocidalo},
  journal={Cellular and Molecular Life Sciences CMLS},
  year={1997},
  volume={53},
  pages={864-870}
}
Abstract. Infection by the human immunodeficiency virus (HIV-1) causes chronic ongoing inflammation in HIV-1 seropositive individuals as shown by high plasma levels of inflammatory cytokines and production of reactive oxygen intermediates (ROIs). One source of ROIs is provided from the very early stages of HIV infection by activated polymorphonuclear neutrophils. Tat, the viral protein, is also specifically responsible for an endogenous cellular increase of ROI. In this review we also evaluate… 

Redox and Activation Status of Monocytes from Human Immunodeficiency Virus-Infected Patients: Relationship with Viral Load

TLDR
Alterations of adhesion molecule expression and increased actin polymerization could play a role in transendothelial migration of these activated monocytes in HIV-infected patients at different stages of the disease.

The role of phagocytes in HIV-related oxidative stress.

Amplification of the Inflammatory Cellular Redox State by Human Immunodeficiency Virus Type 1-Immunosuppressive Tat and gp160 Proteins

TLDR
The immunosuppressive effects of HIV-1 Tat and gp160 proteins and oxidative stress are correlated, since the native but not the inactivated Tat andgp160 proteins inhibit the cellular immune response and enhance oxidative stress, consistent with a role of the membrane NADPH oxidation in the cellular response to immune activation.

Redox-driven events in the human immunodeficiency virus type 1 (HIV-1) infection and their clinical implications.

TLDR
This review aims to characterize the redox-driven events in the HIV-1 infection and their clinical implications in the disease features.

A Key Role for HIV-1-Activated NADPH Oxidase in the Pathogenesis of AIDS

TLDR
The observation that the prevalence of HIV-1 infection is anomalously low (for sub-Sahara Africa) among populations near Lake Chad which regularly consume spirulina, should further encourage studies to evaluate the therapeutic and preventive potential of Spirulina or PCB with respect to HIV- 1 infection.

Activation of the Oxidative Stress Pathway by HIV-1 Vpr Leads to Induction of Hypoxia-inducible Factor 1α Expression*

TLDR
The results point to the activation of hypoxia-inducible factor 1 (HIF-1) upon HIV-1 infection and its elevation in brain cells of AIDS patients with dementia and that, by inducing oxidative stress via activation of Hif-1, Vpr can induce HIV- 1 gene expression and dysregulate multiple host cellular pathways.

HIV-1 Env induces pexophagy and an oxidative stress leading to uninfected CD4+ T cell death

TLDR
It is demonstrated that Env-induced oxidative stress is responsible for the death by apoptosis of bystander CD4+ T lymphocytes in HIV-1-infected patients, and peroxisomes, organelles involved in the control of oxidative stress, are targeted by EnV-mediated autophagy.

Mechanisms of neutrophil death in human immunodeficiency virus‐infected patients: role of reactive oxygen species, caspases and map kinase pathways

Neutrophils from human immunodeficiency virus‐positive (HIV+) patients have an increased susceptibility to undergo programmed cell death (PCD), which could explain neutropenia during advanced
...

References

SHOWING 1-10 OF 54 REFERENCES

Cytokines in HIV infection.

Appraisal of potential therapeutic index of antioxidants on the basis of their in vitro effects on HIV replication in monocytes and interleukin 2-induced lymphocyte proliferation.

TLDR
The effects of BHA and NAC on the regulation of HIV-1 expression in latently infected U1 cells and in productively and chronically infected U937 cells and the suppressive effect on immune functions in vitro warrant prudence in the design of antioxidant-based therapies aimed at suppressing HIV replication.

Fas antigen stimulation induces marked apoptosis of T lymphocytes in human immunodeficiency virus-infected individuals

TLDR
Findings show that CD4+ and CD8+ T lymphocytes in HIV-infected individuals are primed in vivo to undergo apoptosis in response to Fas stimulation, suggesting that Fas signaling may be responsible for the T lymphocyte functional defects and depletion observed in HIV disease.

Prevention of early cell death in peripheral blood lymphocytes of HIV infected individuals by an anti-oxidant: N-Acetyl-Cysteine

TLDR
N-Acetyl-Cystein administration to HIV seropositive patients seems to prevent early cell death and to lead an “overprotection” of patients’ PBLs.

Inhibition of HIV‐1 replication and NF-x B activity by cysteine and cysteine derivatives

TLDR
The experiments in this report show that cysteine or N-acetylcysteine (NAC) raise the intracellular glutathione (GSH) level and inhibit HIV-1 replication in persistently infected Molt-4 and U937 cells, but inhibition of HIV- 1 replication appears not to be directly correlated with CSH levels.

Suppression of human immunodeficiency virus expression in chronically infected monocytic cells by glutathione, glutathione ester, and N-acetylcysteine.

TLDR
The present findings, which elucidate relationships between cellular GSH and HIV expression, suggest that therapy with thiols may be of value in the treatment of HIV infection.

Cytokine-stimulated human immunodeficiency virus replication is inhibited by N-acetyl-L-cysteine.

TLDR
Because NAC reverses tumor necrosis factor alpha toxicity both in cells and in animals and is a well-known drug that can be administered orally without known toxicity in humans, these results suggest that NAC is a possible therapeutic agent in AIDS.

Intracellular glutathione levels in T cell subsets decrease in HIV-infected individuals.

TLDR
It is shown that relative GSH levels in CD4+ and CD8+ T cells from HIV+ individuals are significantly lower than in corresponding subsets from uninfected controls, suggesting that low intracellular GSH Levels may be an important factor in HIV infection and in the resulting immunodeficiency.

Apoptosis occurs predominantly in bystander cells and not in productively infected cells of HIV- and SIV-infected lymph nodes

TLDR
It is shown, using in situ labelling of lymph nodes from HIV- infected children and SIV-infected macaques, that apoptosis occurs predominantly in bystander cells and not in the productively infected cells themselves, arguing that rational drug therapy may involve combination agents targeting viral replication in infected cells and apoptosis of uninfected cells.

Sensitization of T cells to CD95-mediated apoptosis by HIV-1 Tat and gp120

TLDR
It is shown here that HIV-1 Tat strongly sensitizes TCR- and CD4(gpl20)-induced apoptosis by upregulation of CD95 ligand expression, a mechanism that may contribute to CD4+ T-cell depletion in AIDS.
...