RT Journal Article
T1 Massive Release of CD9+ Microvesicles in Human Immunodeficiency Virus Infection, Regardless of Virologic Control.
A1 Poveda, Eva
A1 Tabernilla, Andrés
A1 Fitzgerald, Wendy
A1 Salgado-Barreira, Ángel
A1 Grandal, Marta
A1 Pérez, Alexandre
A1 Mariño, Ana
A1 Álvarez, Hortensia
A1 Valcarce, Nieves
A1 González-García, Juan
A1 Bernardino, José Ignacio
A1 Gutierrez, Félix
A1 Fujioka, Hisashi
A1 Crespo, Manuel
A1 Ruiz-Mateos, Ezequiel
A1 Margolis, Leonid
A1 Lederman, Michael M
A1 Freeman, Michael L
K1 HIV
K1 elite controllers
K1 extracellular vesicles
K1 microvesicles
K1 mitochondria
AB 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.
YR 2022
FD 2022
LK http://hdl.handle.net/10668/19805
UL http://hdl.handle.net/10668/19805
LA en
DS RISalud
RD Apr 7, 2025