Individuals infected with HIV exhibit both severe immune deficiency and aberrant inflammation, resulting in susceptibility to secondary infections.

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A high viral load is associated with a dampened inflammatory response in innate immune cells from HIV-infected individuals.
Compared to cells collected prior to the initiation of ART, innate immune cells collected after patients started ART exhibited an increased response to inflammatory stimuli. Compared to other factors, patient viral load was the most predictive of the innate immune cell response. In monocytes, epigenetic modifications were observed at the locus of the gene encoding pro-inflammatory cytokine TNFα that associated with high levels of virus.
Together, the results of this study identify viral load as a driver of innate immune dysfunction in HIV-infected individuals.
Source-Eurekalert
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