Timely Topics in Clinical Immunology

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Oxidative Stress In HIV Infection Research Articles

 

HIV-induced oxidative stress plays a crucial role within the development of a good spectrum of virus-associated pathologies. Among them are neurotoxicity and dementia and immune imbalance with the exhaustion of the pool of CD4 T-lymphocytes, as well as lung and cardiovascular disorders.

Numerous lines of evidence show that HIV infection triggers pronounced oxidative stress in both laboratory models and therefore the context of in vivo infection. HIV-infected individuals exhibit enhanced ROS production in monocytes and severely elevated levels of oxidized nucleic bases such as 8-oxoG and lipid peroxidation products, including MDA in plasma and alkanes in the breath output.

Compensation of the pathogenic effects of HIV-1 replication requires intact functions of ROS detoxifying enzymes. Parsons et al. showed that HIV-1 individuals with a null-allele polymorphism in gstm1 gene, associated with a loss of function of the Phase II detoxifying enzyme glutathione S-transferase, exhibit lower count of CD4 T-cells, increased HIV viral load, and increased 8-oxoG in mitochondrial DNA. However, HIV-infected individuals demonstrate a discount of total antioxidant capacity, decreased GSH/GSSG ratio in epithelial lung fluid [3], and decreased GSH content in blood.

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