---
title: "Extracellular vesicle signatures linked to CMV, EBV, and HHV‑6 reactivation after haploidentical H"
id: "frontiers-in-immunology-7-extracellular-vesicle-phenotypic-patterns-associated-with-cmv-ebv-and-hhv-6"
canonical_url: "https://medichelpline.com/clinical-feed/frontiers-in-immunology-7-extracellular-vesicle-phenotypic-patterns-associated-with-cmv-ebv-and-hhv-6"
content_type: "clinical_feed_article"
specialty: "Infectious Disease"
source_name: "Frontiers in Immunology"
source_url: "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1937675"
published_at: "2026-10-05T00:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Extracellular vesicle signatures linked to CMV, EBV, and HHV‑6 reactivation after haploidentical H
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/frontiers-in-immunology-7-extracellular-vesicle-phenotypic-patterns-associated-with-cmv-ebv-and-hhv-6
- **Specialty:** [Infectious Disease](https://medichelpline.com/clinical-feed/infectious-disease.md)
- **Primary Source:** Frontiers in Immunology
- **Source URL:** [Original Journal Publication](https://www.frontiersin.org/articles/10.3389/fimmu.2026.1937675)
- **Published At:** 2026-10-05T00:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- This exploratory biomarker discovery study analyzed circulating **extracellular vesicles (EVs)** in 32 consecutive recipients of haploidentical hematopoietic cell transplantation (hHCT) who received post‑transplant cyclophosphamide (PT‑Cy). EV surface marker profiles were measured by flow cytometry before transplant and at predefined timepoints through the first three months post‑HCT. - Viral monitoring by qPCR in whole blood was performed weekly; reactivation was defined as viral DNA >1000 IU/mL. CMV reactivation occurred in 20 patients, EBV in 11, and HHV‑6 in 17. Pre‑emptive CMV therapy was started at >4000 IU/mL per local practice. - Multivariable and time‑varying Cox regression models identified distinct EV phenotypic patterns associated with each virus. **CMV** reactivation associated with higher EV expression of **CD44, CD86, CD140a (PDGFRα)**, and **CD144**. - **EBV** reactivation associated with lower concentrations of **CD30**‑positive EVs and higher **KRT18** expression on EVs. - **HHV‑6** reactivation associated with altered EV profiles including **CD26, CD86, CD120a,** and **CD144**. - These EV–virus associations persisted after adjustment for acute graft‑versus‑host disease (aGvHD) and concomitant viral events, suggesting EV phenotypes may reflect virus‑specific host biology rather than solely GvHD effects. - EVs were isolated from plasma, characterized by electron microscopy, nanoparticle tracking analysis, and Western blot for EV markers and contaminants. Flow cytometry used a predefined antibody panel (including tetraspanins CD9/CD81) previously developed for this cohort; the detection window favored larger EVs. - The authors conclude circulating EV phenotypes are candidate biomarkers that warrant external validation for predicting and monitoring herpesvirus reactivation after hHCT.
## Clinical Analysis & Structured Key Points
Frontiers | Extracellular vesicle phenotypic patterns associated with CMV, EBV and HHV-6 reactivation after haploidentical transplantation with post-transplant cyclophosphamide ORIGINAL RESEARCH article Front. Immunol. , 05 October 2026 Sec. Alloimmunity and Transplantation Volume 17 - 2026 | https://doi.org/10.3389/fimmu.2026.1937675 Published in Frontiers in Immunology Alloimmunity and Transplantation 7 impact factor 11.3 citescore Editor & Reviewers Edited by B H Brian H Johnstone Reviewed by M E Mohamed Eltokhy W Y Wen Yin Outline Figures and Tables Figure 1 View in article Figure 2 View in article Figure 3 View in article Figure 4 View in article Table 1 Patient and transplant characteristics. View in article Table 2 Multivariable association analyses between EV surface marker levels and viral infections/reactivations, with bootstrap-based assessment of marker-selection stability across post-HCT time periods. View in article Table 3 Effect of opportunistic viral infections/reactivations and aGvHD on biomarker association. View in article Table 4 Biomarker performance at different times after hHCT. View in article ORIGINAL RESEARCH article Front. Immunol. , 05 October 2026 Sec. Alloimmunity and Transplantation Volume 17 - 2026 | https://doi.org/10.3389/fimmu.2026.1937675 Extracellular vesicle phenotypic patterns associated with CMV, EBV and HHV-6 reactivation after haploidentical transplantation with post-transplant cyclophosphamide G L Giuseppe Lia 1,2 ‡ C D Clara Di Vito 3,4 ‡ S B Stefania Bruno 5 J M Jacopo Mariotti 6 A M Alessia Melis 2 M C Michela Calvi 3,4 L G Luisa Giaccone 1,2 A S Armando Santoro 6 S B Stefania Bramanti 6 L C Luca Castagna 6 † A E Andrea Evangelista 7 D M Domenico Mavilio 3,4 +4 more B B Benedetto Bruno 1,2 * 1. Division of Hematology, Department of Oncology, A.O.U. Città della Salute e della Scienza di Torino, Torino, Italy 2. Department of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy 3. Department of Medical Biotechnologies and Translational Medicine (BioMeTra), University of Milan, Milan, Italy 4. Unit of Clinical and Experimental Immunology, Istituti di Ricovero e Cura a Carattere Scientifico (IRCCS) Humanitas Research Hospital, Rozzano, Milan, Italy 5. Department of Medical Sciences, University of Torino, Torino, Italy 6. Bone Marrow Transplant Unit, IRCCS Humanitas Research Hospital, Milan, Italy 7. Clinical Epidemiology, A.O.U. Città della Salute e della Scienza di Torino, Torino, Italy See more Article metrics View details Abstract Introduction: Human cytomegalovirus (CMV), Epstein–Barr virus (EBV), and human herpesvirus 6 (HHV-6) remain important causes of morbidity after allogeneic hematopoietic cell transplantation (HCT), yet biomarkers predicting viral reactivation are lacking. Extracellular vesicles (EVs) have emerged as promising liquid-biopsy tools in inflammatory and infectious diseases. Methods: In this exploratory biomarker discovery study, 32 consecutive recipients of haploidentical HCT with post-transplant cyclophosphamide were prospectively enrolled. EV surface marker profiles were assessed by flow cytometry before transplantation and at predefined time points during the first three months post-HCT. Associations between EV phenotypes and viral reactivation were evaluated using logistic regression and time-varying Cox models. Results: CMV, EBV, and HHV-6 reactivation occurred in 20, 11, and 17 patients, respectively. Multivariable analyses showed that different EV phenotypic patterns were associated with CMV, EBV, and HHV-6 reactivation. CMV reactivation was associated with increased EV expression of CD44, CD86, CD140a, and CD144. EBV reactivation correlated with reduced CD30-positive EV concentrations and increased KRT18 expression. HHV-6 reactivation was associated with altered CD26, CD86, CD120a, and CD144 EV profiles. These associations remained significant after adjustment for acute graft-versus-host disease and concomitant viral infections. Discussion: Collectively, these exploratory findings support further validation of circulating EV phenotypes as candidate biomarkers for predicting and monitoring viral reactivation after haploidentical HCT. 1 Introduction Haploidentical hematopoietic stem cell transplantation (hHCT) with post-transplant cyclophosphamide (PT-Cy) is an effective and widely accessible curative option for patients with high-risk hematologic malignancies. The adoption of reduced-intensity conditionings has expanded its feasibility to older or medically unfit individuals ( 1 ). However, viral infections cause significant morbidity, particularly reactivation of latent herpesviruses. Among these, human Cytomegalovirus (CMV) represents the most clinically relevant pathogen, contributing to transplant-related complications, including multi-organ disease, graft dysfunction, and increased susceptibility to secondary infections ( 2 , 3 ). Several risk factors predispose to CMV reactivation, including immunosuppression intensity, donor–recipient serostatus, conditioning regimen, T-cell depletion strategies, and acute graft-versus-host disease (aGvHD) ( 4 ). CMV exhibits broad cellular tropism, infecting endothelial, epithelial, smooth muscle cells, fibroblasts, leukocytes, and dendritic cells ( 5 ) through viral complexes, including gH/gL/pUL128-pUL130-pUL131A and gH/gL/gO ( 5 – 7 ). CMV entry is mediated by several host membrane proteins, including EGFR, integrins, heparan sulfate, THY-1, and particularly PDGFRα (CD140α), which has emerged as a key determinant of viral infection ( 8 , 9 ). Endothelial cells (ECs) play a central role in CMV pathogenesis, persistence and dissemination, serving as viral reservoirs ( 10 ) and exhibiting functional alterations such as increased permeability and upregulation of adhesion molecules including CD44 ( 11 ). Other herpesviruses, particularly Epstein-Barr virus (EBV) and Human Herpesvirus 6 (HHV6), also commonly infect or reactivate post-hHCT ( 12 , 13 ). EBV, a gamma-herpesvirus, displays a dual tropism for B cells and epithelial cells, alternating between latent infection of memory B cells and lytic replication in epithelial tissues. Viral entry involves gp350/220 binding to CD21/CD35, core fusion proteins gH/gL/gB, and gp42-mediated engagement of HLA class II molecules ( 14 – 18 ). HHV6 infects nearly all individuals in early life and persists lifelong with tropism for hematopoietic cells, including CD34+ progenitors ( 17 , 18 ). It can infect multiple immune cell types and endothelial cells, inducing proinflammatory cytokine release and impairing immune function ( 19 – 21 ). HHV6 reactivation has been associated with delayed engraftment, impaired T-cell reconstitution, increased co-infections, and severe GvHD post-HCT ( 22 – 26 ). Although quantitative PCR monitoring enables early detection of viral replication, biomarkers reflecting the biological processes preceding viral reactivation remain limited ( 2 , 3 , 12 , 13 ). Extracellular vesicles (EVs) have emerged as promising liquid-biopsy tools in inflammation, tissue injury, malignancies, and viral infections ( 24 – 31 ). EVs released by infected cells may carry altered host-derived molecules and potentially reflect early virus-induced perturbations before clinically detectable infection ( 25 – 29 ). We previously generated longitudinal EV immunophenotyping dataset in a cohort of haploidentical HCT recipients to investigate acute GvHD ( 32 ). In the present study, we performed a secondary analysis of the same patient cohort, longitudinal sampling schedule, and EV dataset, applying a distinct clinical stratification and analytical framework to investigate the relationship between EV phenotypes and CMV, EBV, and HHV-6 reactivation after transplantation. Specifically, we sought to determine whether circulating EV signatures reflect virus-associated biological pathways and whether they may serve as early indicators of subsequent viral reactivation, thereby laying the groundwork for the development of novel biological risk-stratification strategies in the post-transplant setting. 2 Materials and methods 2.1 Patients, transplant characteristics, viral infection/reactivation Thirty-two consecutive patients undergoing hHCT were enrolled at the Bone Marrow Transplant Unit, Humanitas Cancer Center, Humanitas Research Hospital, Rozzano, Milan, Italy, before the introduction of Letermovir in Italy (2019). All patients and donors provided written informed consent. Plasma samples were prospectively collected under institutional biological repository guidelines and stored for EV analyses ( Figure 1 ). Patient and transplant characteristics are summarized in Table 1 . GvHD prophylaxis consisted of PT-Cy 50 mg/kg on days +3 and +4, tacrolimus and/or cyclosporin A, and mycophenolate mofetil (MMF) from day +5. Granulocyte colony-stimulating factor (G-CSF) was started on day +5. Disease response followed the European Bone Marrow Transplantation (EBMT) Group criteria. To identify patients experiencing CMV, EBV, and/or HHV-6 infection/reactivation post-hHCT, viral loads were tested weekly in whole blood (PB) using real-time PCR (CMV R-GENE, EBV R-GENE, HHV-6 R-GENE, Argene, Biomérieux). For study purposes, reactivation was defined as DNA exceeding 1000 IU/mL post-transplantation. This threshold captures early viral replication and may differ from thresholds used in routine clinical practice. CMV pre-emptive antiviral therapy (Foscarnet 90 mg/kg, Ganciclovir 5 mg/kg, or Valganciclovir twice daily for 2 weeks) was initiated above 4000 IU/mL viral load. No pre-emptive therapy was administered for EBV or HHV-6 unless clinically indicated. GvHD was diagnosed according to the Glucksberg grading system. Figure 1 Study design and timing of extracellular vesicle sampling, virologic monitoring, and viral reactivation events. Peripheral blood samples for extracellular vesicle (EV) analyses were collected before transplantation (day −6), at transplantation (day 0), and at predefined time points after haploidentical hematopoietic cell transplantation (hHCT) with post-transplant cyclophosphamide (days +3, +7, +14, +21, +30, +45, and months 2, 2.5, and 3). The number of evaluated patients (N) at each time point is indicated below the timeline. Patients underwent routine weekly quantitative PCR monitoring for cytomegalovirus (CMV), Epstein–Barr virus (EBV), and human herpesvirus 6 (HHV-6) throughout the post-transplant period. Dashed vertical lines indicate the median time to viral reactivation observed in the study cohort: day +34 for HHV-6, day +50 for CMV, and day +94 for EBV. The image illustrates the temporal relationship between EV sampling, virologic surveillance, and the occurrence of viral reactivation events analyzed in this exploratory study. The schedule of EV assessments was aligned with routine weekly virologic surveillance, which also served as the basis for the 7-day interval analyses. Table 1 N Sex: d/r r: age d: age Disease Conditioning regimen Stem cell source aGvHD Gluk grade; day post-hHCT CMV react; day post-hHCT EBV react; day post- hHCT HHV6 react; day post-hHCT 11 F 34 29 HL RIC, Baltimore BM 2; 33 0 1; 84 1; 40 12 F 44 23 NHL RIC, Baltimore BM 0 0 0 1; 39 13 M 54 46 NHL RIC, Baltimore BM 1; 92 1; 50 0 0 14 F 57 24 HL RIC, Baltimore BM 0 0 0 1; 31 15 F 57 62 NHL RIC, Baltimore BM 2; 68 1; 48 0 1; 40 16 F 24 60 HL RIC, Baltimore BM 0 0 0 0 17 M 24 45 HL RIC, Baltimore BM 0 1; 49 1; 94 0 18 M 25 51 NHL RIC, Baltimore BM 1; 40 0 1; 103 0 19 M 47 38 HL RIC, Baltimore BM 0 1; 33 1; 54 0 20 M 51 50 NHL RIC, Baltimore BM 0 1; 51 1; 216 0 21 F 28 32 HL RIC, Baltimore BM 0 1; 275 0 0 22 M 25 21 HL RIC, Baltimore BM 1; 75 0 1; 89 0 23 F 26 54 HL RIC, Baltimore BM 0 0 0 0 25 M 62 35 NHL RIC, Baltimore BM 2; 34 1; 63 0 1; 34 26 F 42 49 NHL RIC, Baltimore BM 1; 30 1; 65 1; 314 0 27 F 40 48 HL RIC, Baltimore BM 0 1; 29 1; 122 0 28 F 21 52 HL RIC, Baltimore BM 1; 41 0 1; 55 0 29 M 24 51 HL RIC, Baltimore BM 0 1; 53 0 0 30 F 27 43 HL RIC, ONC005 BM 1; 57 0 0 0 32 M 32 57 HL RIC, ONC005 BM 0 1; 29 0 0 33 M 37 47 HL MAC, TFB BM 0 0 0 1; 40 35 M 30 22 HL RIC, Baltimore BM 0 1; 53 0 1; 30 36 F 66 71 HL RIC, ONC005 BM 0 1; 56 0 0 38 M 44 27 NHL MAC, TBF BM 0 1; 42 0 1; 18 39 M 50 44 AML MAC, TTFBx3 PBSC 0 0 0 1; 11 40 M 55 56 HL RIC, ONC005 BM 4; 49 1; 54 0 1; 34 41 F 37 71 NHL RIC, ONC005 BM 0 1; 34 0 1; 22 42 F 46 35 ALL MAC, TBF BM 2; 92 1;102 1; 147 1; 280 44 M 61 36 NHL RIC, Baltimore BM 2; 38 1; 10 0 1; 14 46 M 50 46 CLL RIC, Baltimore BM 0 1; 153 0 1; 138 47 F 47 45 NHL RIC, Baltimore BM 2; 41 1; 50 0 1; 50 48 M 24 51 ALL MAC, TBF BM 1; 80 0 1; 55 1; 13 Patient and transplant characteristics. d, donor; r, recipient; HL, Hodgkin Lymphoma; NHL, non-Hodgkin Lymphoma; AML, Acute Myeloid Leukemia; ALL, Acute Lymphoid Leukemia; CLL, Chronic Lymphoid Leukemia; RIC, Reduce Intensity Conditioning; MAC, Myeloablative Conditioning; Baltimore, Fludarabine (30mg/m2; days -6, -5, -4, -3, -2), Cyclophosphamide (14, 5 mg/Kg; days -6, -5), Total Body Irradiation (200 cGy); TBF, Thiotepa (5 mg/Kg; days -6, -5), Fludarabine (50 mg/m2; days -4, -3, -2), Busulphan (30 mg/Kg; days -4, -3, -2); ONC005, Thiotepa (5 mg/Kg twice a day; day -6), Fludarabine (30mg/m2; days -5; -4, -3, -2), Cyclophosphamide (30 mg/Kg; days -5); BM, Bone Marrow; PBSC, Peripheral Blood Stem Cells; aGvHD, acute Graft versus Host Disease; CMV react, Cytomegalovirus reactivation; EBV react, Epstein Barr Virus reactivation; HHV6 react, Human Herpesvirus-6 reactivation; 0, no reactivation; 1, reactivation. 2.2 Plasma sample collection PB samples were collected in Lithium-Heparin tubes from recipients before transplant (day -6) and from recipients at different time-points post-transplant (median, Figure 1 ). Plasma samples were obtained after mononuclear cell separation by density-gradient centrifugation (Lympholyte-H, Cedarlane, Burlington, Canada) and stored at -80 °C. 2.3 Extracellular vesicle precipitation and characterization To remove platelet contamination, plasma samples (~1 ml) were thawed on ice and centrifuged at 2000 × g for 40 minutes at 4 °C. EVs were then precipitated ( 30 ), resuspended in 150 μL of Roswell Park Memorial Institute (RPMI) medium supplemented with Penicillin (100 U/L), Streptomycin (100 mg/L), Amphotericin B (0.25 mg/L) (EUROCLONE Spa, Pero, MI, Italy), and 10% Dimethyl sulfoxide (DMSO), and stored at -80 °C. All samples underwent a single freeze-thaw cycle before analysis. EV integrity was confirmed by transmission electron microscopy and nanoparticle tracking analysis (NTA). EVs were allowed to adhere to 200-mesh nickel formvar carbon-coated grids (Electron Microscopy Sciences, Hatfield, Pennsylvania, USA) for 10 minutes. Grids were washed with Phosphate-Buffered Saline (PBS, pH 7.4), fixed with 2.5% glutaraldehyde containing 2% sucrose, negatively stained with NanoVan (Nanoprobes, Yaphank, New York, USA), and examined using a Jeol JEM 1400 Flash electron microscope (Tokyo, Japan). EV size and concentration were assessed by NTA. EV preparations were diluted (1:3000) in sterile saline solution (0.9% NaCl). Brownian motion under laser illumination was recorded (three 30-second videos) using a NanoSight NS300 system (NanoSight Ltd., Minton Park, United Kingdom). Data were analyzed using Nanosight NTA 3.2 software, applying the Stokes-Einstein equation ( 31 ). Western blot analysis was performed on EVs precipitated from plasma samples using PEG/protamine to evaluate EV enrichment and the potential co-isolation of non-vesicular components. EV proteins were isolated by lysis for 30 min at 4 °C in RIPA buffer (20 mM Tris-HCl, 150 mM NaCl, 1% deoxycholate, 0.1% SDS, 1% Triton X-100, pH 7.8) supplemented with 1% phenylmethylsulfonyl fluoride and 1% protease and phosphatase inhibitor cocktail (all from Sigma-Aldrich). Protein concentration was quantified using the BCA Protein Assay Kit (Pierce™, Thermo Fisher Scientific, Waltham, MA, USA). Protein samples (30 µg) were separated under reducing conditions on 4–20% gradient Mini-PROTEAN TGX precast gels (Bio-Rad, Hercules, CA, USA) and transferred onto 0.2-µm nitrocellulose membranes using the Trans-Blot Turbo Transfer System (Bio-Rad). Membranes were blocked for 2 h at room temperature in PBS-T containing 0.1% Tween-20 and 5% bovine serum albumin (BSA). They were then incubated for 18 h at 4 °C with primary antibodies, all purchased from Cell Signaling Technology (Danvers, MA, USA). The primary antibodies used included: rabbit anti-GM130 (as a negative control); rabbit anti-TSG101 and anti-CD63 (as EV-specific markers); rabbit anti-ApoB (to evaluate apolipoprotein contamination). After extensive washing, the membranes were incubated for 1 h at room temperature with the appropriate peroxidase-conjugated secondary antibodies (Invitrogen, Thermo Fisher Scientific). Chemiluminescent signals were detected using ECL substrate (Bio-Rad) and acquired with the ChemiDoc Imaging System (Bio-Rad). 2.4 EV immunophenotyping The complete EV immunophenotyping dataset analyzed in the present study originated from the same experimental cohort and flow cytometry acquisitions previously reported ( 32 ). No additional flow cytometry measurements were performed, and no new biomarkers were added to the original EV panels. Instead, the existing longitudinal dataset was reanalyzed using a distinct clinical stratification and statistical framework specifically designed to investigate the relationship between EV signatures and CMV, EBV, and HHV-6 reactivation after hHCT. In the original dataset, EVs were characterized by flow cytometry using fluorescein isothiocyanate (FITC)- or phycoerythrin (PE)-conjugated antibodies ( Supplementary Table S1 ). The antibody panel was predefined in our previous studies ( 30 , 32 ) and was not specifically developed for viral reactivation. It included markers related to immune activation, endothelial biology, and epithelial injury. Because these biological processes may also accompany post-HCT viral reactivation, the same panel was explored in the present secondary analysis without introducing additional markers. CD9 and CD81 were evaluated as EV-associated tetraspanins to identify tetraspanin-positive events within the detectable EV-enriched fraction; their expression was not considered evidence of a specific exosomal origin. Mouse non-immune isotypic FITC or PE IgGs served as negative controls ( Supplementary Table S1 ). Incubation with tagged antibodies (0.8-1.5 µL) and EVs (3 × 10 9 particles), acquisition on a Guava Instrument (GUAVA easyCyteTM 8, Merck Millipore, Billerica, MA, USA), and gating were performed as previously described ( 32 ). Instrument calibration for small-particle detection was performed using Megamix beads (300 nm, 500 nm, and 3 µm), Megamix-Plus SSC beads (160 nm, 200 nm, 240 nm, and 500 nm), Nanosight-certified size calibration beads (100 nm, 200 nm, and 400 nm), and Apogee beads (110 nm, 590 nm, and 880 nm) to evaluate sub-micron scatter performance. Based on these calibration experiments, the approximate bead-based lower detection threshold was estimated to be 100–150 nm. Because reference beads and biological EVs differ in refractive index and light-scattering properties, this value does not represent an absolute EV size cutoff. The flow cytometric analysis was therefore expected to detect predominantly larger EVs and a proportion of small EVs, whereas the smallest EVs may have remained below the detection threshold ( Supplementary Figure S1 ). For each marker, 5000–10000 events were acquired. Samples were appropriately diluted in filtered FACS flow dilution buffer to ensure a low acquisition speed (<300 events per second) and avoid swarming. Measurements were performed in 2–4 replicates to determine mean fluorescence intensity (MFI), percentage and concentration of marker-positive EVs ( Figure 2 ; Supplementary Figure S2 ) ( 32 ). Concentration of positive EVs was calculated by multiplyi
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