%0 Journal Article
%A Poveda, Eva
%A Tabernilla, Andrés
%A Fitzgerald, Wendy
%A Salgado-Barreira, Ángel
%A Grandal, Marta
%A Pérez, Alexandre
%A Mariño, Ana
%A Álvarez, Hortensia
%A Valcarce, Nieves
%A González-García, Juan
%A Bernardino, José Ignacio
%A Gutierrez, Félix
%A Fujioka, Hisashi
%A Crespo, Manuel
%A Ruiz-Mateos, Ezequiel
%A Margolis, Leonid
%A Lederman, Michael M
%A Freeman, Michael L
%T Massive Release of CD9+ Microvesicles in Human Immunodeficiency Virus Infection, Regardless of Virologic Control.
%D 2022
%U http://hdl.handle.net/10668/19805
%X The role of extracellular vesicles (EVs) in human immunodeficiency virus (HIV) pathogenesis is unknown. We examine the cellular origin of plasma microvesicles (MVs), a type of ectocytosis-derived EV, the presence of mitochondria in MVs, and their relationship to circulating cell-free mitochondrial deoxyribonucleic acid (ccf-mtDNA) in HIV-infected patients and controls. Five participant groups were defined: 30 antiretroviral therapy (ART)-naive; 30 ART-treated with nondetectable viremia; 30 elite controllers; 30 viremic controllers; and 30 HIV-uninfected controls. Microvesicles were quantified and characterized from plasma samples by flow cytometry. MitoTrackerDeepRed identified MVs containing mitochondria and ccf-mtDNA was quantified by real-time polymerase chain reaction. Microvesicle numbers were expanded at least 10-fold in all HIV-infected groups compared with controls. More than 79% were platelet-derived MVs. Proportions of MVs containing mitochondria (22.3% vs 41.6%) and MV mitochondrial density (706 vs 1346) were significantly lower among HIV-infected subjects than controls, lowest levels for those on ART. Microvesicle numbers correlated with ccf-mtDNA levels that were higher among HIV-infected patients. A massive release of platelet-derived MVs occurs during HIV infection. Some MVs contain mitochondria, but their proportion and mitochondrial densities were lower in HIV infection than in controls. Platelet-derived MVs may be biomarkers of platelet activation, possibly reflecting pathogenesis even in absence of HIV replication.
%K HIV
%K elite controllers
%K extracellular vesicles
%K microvesicles
%K mitochondria
%~