Miguel A. Pesqueira Sanchez
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Miguel A. Pesqueira Sanchez has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Emily A. Fehrman
Department of Medicine, University of California, San Francisco, San Francisco, CA 94110, USA
1 shared publication - Jeffrey N. Martin
Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA, USA
1 shared publication - John Daniel Kelly
Department of Epidemiology and Biostatistics, University of California, San Francisco, USA
1 shared publication - Michael J. Peluso
Division of HIV, Infectious Diseases, and Global Medicine, University of California, San Francisco, USA
1 shared publication - Pahul S. Chhabra
Department of Medicine, University of California, San Francisco, San Francisco, CA 94110, USA
1 shared publication - Rosalia de Necochea Campion
Aethlon Medical, Inc., San Diego, CA 92121, USA
1 shared publication
Latest Publications
- Open Access
- 25 June 2026
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 27 (13) , 5723
Increased Mannosylation of Extracellular Vesicles in Long COVID Plasma as a Binding Target for Galanthus nivalis Agglutinin (GNA) Affinity Resin
There is no proven therapy for Long COVID, a post-acute condition characterized by persistent symptoms following SARS-CoV-2 infection. Extracellular vesicles (EVs) are emerging as mediators of disease pathogenesis through their molecular cargo. We investigated whether EV glycosylation is altered in Long COVID plasma and whether these vesicles can be selectively targeted using a glycan-binding affinity resin. Large (100–500 nm) and small (40–200 nm) EVs were isolated from post-acute COVID-19 plasma and analyzed by nanoparticle flow cytometry to assess surface glycosylation. Small EV capture assays were performed using Galanthus nivalis agglutinin (GNA) affinity resin. Plasma miRNA profiles before and after GNA treatment were evaluated using NanoString nCounter analysis, and potential downstream pathway effects were computationally inferred using validated miRNA–mRNA interactions and PROGENy. Mannose-positive large EVs were significantly increased in Long COVID compared to recovered controls (p < 0.05). GNA-mediated small EV capture correlated with mannose-positive EV abundance (r = 0.341, p < 0.05), and seven miRNAs were significantly reduced following treatment. Computational pathway analysis suggested modulation of key signaling pathways, including JAK-STAT, Estrogen, VEGF, and PI3K. These findings suggest a glycan-associated EV signature in Long COVID and support further investigation of lectin-based capture as a potential strategy to target vesicle-associated molecular cargo.
- 25 June 2026
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 27 (13) , 5723
Open AccessIncreased Mannosylation of Extracellular Vesicles in Long COVID Plasma as a Binding Target for Galanthus nivalis Agglutinin (GNA) Affinity Resin
There is no proven therapy for Long COVID, a post-acute condition characterized by persistent symptoms following SARS-CoV-2 infection. Extracellular vesicles (EVs) are emerging as mediators of disease pathogenesis through their molecular cargo. We investigated whether EV glycosylation is altered in Long COVID plasma and whether these vesicles can be selectively targeted using a glycan-binding affinity resin. Large (100–500 nm) and small (40–200 nm) EVs were isolated from post-acute COVID-19 plasma and analyzed by nanoparticle flow cytometry to assess surface glycosylation. Small EV capture assays were performed using Galanthus nivalis agglutinin (GNA) affinity resin. Plasma miRNA profiles before and after GNA treatment were evaluated using NanoString nCounter analysis, and potential downstream pathway effects were computationally inferred using validated miRNA–mRNA interactions and PROGENy. Mannose-positive large EVs were significantly increased in Long COVID compared to recovered controls (p < 0.05). GNA-mediated small EV capture correlated with mannose-positive EV abundance (r = 0.341, p < 0.05), and seven miRNAs were significantly reduced following treatment. Computational pathway analysis suggested modulation of key signaling pathways, including JAK-STAT, Estrogen, VEGF, and PI3K. These findings suggest a glycan-associated EV signature in Long COVID and support further investigation of lectin-based capture as a potential strategy to target vesicle-associated molecular cargo.