Abstract
The infection of CD4 T-lymphocytes with human immunodeficiency virus (HIV), the etiological agent of acquired immunodeficiency syndrome (AIDS), disrupts cellular homeostasis, increases oxidative stress and interferes with micronutrient metabolism. Viral replication simultaneously increases the demand for micronutrients and causes their loss, as for selenium (Se). In HIV-infected patients, selenium deficiency was associated with a lower CD4 T-cell count and a shorter life expectancy. Selenium has an important role in antioxidant defense, redox signaling and redox homeostasis, and most of these biological activities are mediated by its incorporation in an essential family of redox enzymes, namely the selenoproteins. Here, we have investigated how selenium and selenoproteins interplay with HIV infection in different cellular models of human CD4 T lymphocytes derived from established cell lines (Jurkat and SupT1) and isolated primary CD4 T cells. First, we characterized the expression of the selenoproteome in various human T-cell models and found it tightly regulated by the selenium level of the culture media, which was in agreement with reports from non-immune cells. Then, we showed that selenium had no significant effect on HIV-1 protein production nor on infectivity, but slightly reduced the percentage of infected cells in a Jurkat cell line and isolated primary CD4 T cells. Finally, in response to HIV-1 infection, the selenoproteome was slightly altered.
Highlights
The human immunodeficiency virus (HIV) is an enveloped, linear, positive-sense single-stranded RNA virus that belongs to the family of Retroviridae (Group VI), genusLentivirus
AlAlthough it is well established that the selenoproteome is extent, highly regulated by selethough it is well that models, the selenoproteome highlyabout regulated by selenium nium availability in established several cellular very little is is known the expression patavailability in several cellular models, very little is to known aboutsupplementation the expression pattern of tern of these selenoproteins and their response selenium in human these selenoproteins and their response to selenium supplementation in human immune cells, and
Since the selenoproteome of primary CD4 T-cells isolated from healthy donors seemed well responsive to selenium level variations and different from Jurkat cells’ selenoproteome, we investigated whether selenium modified HIV-1 infection in this model
Summary
The human immunodeficiency virus (HIV) is an enveloped, linear, positive-sense single-stranded RNA virus that belongs to the family of Retroviridae (Group VI), genus. HIV is the etiological agent of acquired immunodeficiency syndrome (AIDS). Is responsible for a weakened immune system, as it infects immune cells [1]. There are two types of HIV (HIV-1 and HIV-2) that differ in their epidemiological and pathological properties [1]. There are currently more than 37 million people infected with human immunodeficiency virus (HIV), causing about. 1.5 million deaths every year (http://www.who.int/hiv/en/, accessed on 1 December 2021). HIV infection is considered a chronic disease that requires intensive treatment and can present a variable clinical course. HIV-1 infects immune cells that harbor the CD4 receptor and a co-receptor belonging to the chemokine receptor family (CCR5 and CXCR4) [1]
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