Abstract
Extracellular vesicles (EVs) can participate in intercellular communication and pathogenesis. EVs contain many cargos, including proteins, and the composition of EVs differs between cell-types and activation levels. Thus, plasma EVs can be used as a biomarker of systemic response to infection and/or disease progression. In this study, we aimed at describing alterations in the protein content of plasma EVs upon infection with the human T-lymphotropic retrovirus type 1 (HTLV-1). HTLV-1 is the etiological agent of a lymphoproliferative disease (ATL) and a series of inflammatory diseases, including a neurodegenerative inflammatory disease (HAM/TSP). We found that plasma EVs are more abundant and smaller in HTLV-1 asymptomatic carriers or HAM/TSP patients when compared to uninfected healthy donors. Moreover, EVs from HTLV-1 infected donors contain markers of metabolic and mitochondrial stress.
Highlights
Cells release vesicles that can participate in intercellular communication[1]
We aimed to describe the alterations in the protein composition of plasma Extracellular vesicles (EVs) that occur upon human T-lymphotropic virus type 1 (HTLV-1) infection in vivo
We found that plasma from HTLV-1 infected individuals contained significantly more EVs than those from non-infected individuals (NI) donors (Fig. 1C)
Summary
Cells release vesicles that can participate in intercellular communication[1]. extracellular vesicles (EVs) contain biologically active material, which may alter the biology of recipient cells. The composition of EVs differs between cell-types and activation levels; plasma EVs have been used as biomarker of infection or disease[4]. Besides these functions, EVs can be a cellular means to remove misfolded or aggregated proteins, and non-functional organelles[5]. We aimed to describe the alterations in the protein composition of plasma EVs that occur upon HTLV-1 infection in vivo. We found that EVs are more abundant and smaller in the plasma of HTLV-1 infected individuals These EVs contain proteins derived from mitochondria and lysosomes; they are markers of metabolic and mitochondrial stress
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