Thomas A. Angelovich

HIV infection and aging of the innate immune system.

HIV infection induces age-related changes to monocytes and innate immune activation in young men that persist despite combination antiretroviral therapy.

Aging is associated with chronic innate immune activation and dysregulation of monocyte phenotype and function.

Age-associated changes in monocyte and innate immune activation markers occur more rapidly in HIV infected women.

Monocytes as regulators of inflammation and HIV-related comorbidities during cART.

Viremic and Virologically Suppressed HIV Infection Increases Age-Related Changes to Monocyte Activation Equivalent to 12 and 4 Years of Aging, Respectively.

Inflammation-induced foam cell formation in chronic inflammatory disease.

Monocytes from HIV-infected individuals show impaired cholesterol efflux and increased foam cell formation after transendothelial migration.

Ex vivo foam cell formation is enhanced in monocytes from older individuals by both extrinsic and intrinsic mechanisms.

HIV integration and the establishment of latency in CCL19-treated resting CD4(+) T cells require activation of NF-κB.

Persistence of Activated and Adaptive-Like NK Cells in HIV(+) Individuals despite 2 Years of Suppressive Combination Antiretroviral Therapy.

Dysfunctional HDL from HIV+ individuals promotes monocyte-derived foam cell formation in vitro.