Clinical Trial Details
— Status: Completed
Administrative data
| NCT number |
NCT06256341 |
| Other study ID # |
CIRAST HHV-6 |
| Secondary ID |
|
| Status |
Completed |
| Phase |
|
| First received |
|
| Last updated |
|
| Start date |
March 14, 2014 |
| Est. completion date |
November 1, 2023 |
Study information
| Verified date |
February 2024 |
| Source |
Medical University of Graz |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Observational
|
Clinical Trial Summary
Human herpesvirus 6 (HHV-6) causes only minor symptoms in healthy individuals but in
immunosuppressed patients, e.g., patients after allogeneic stem cell transplantation (HSCT),
HHV-6 reactivations can lead to diseases in different organ systems. HHV-6 reactivations have
also been reported to be a cause for delayed engraftment, a trigger of graft-versus-host
disease and a co-factor for other virus reactivations. T-lymphocytes play an important role
in the control of virus reactivations. Little is known about the development of
virus-specific T-cells after allogeneic HSCT.
Description:
Background:
Human herpesvirus 6 (HHV-6) causes only minor symptoms in healthy individuals but in
immunosuppressed patients, e.g., patients after allogeneic stem cell transplantation (HSCT),
HHV-6 reactivations can lead to diseases in different organ systems. HHV-6 reactivations have
also been reported to be a cause for delayed engraftment, a trigger of graft-versus-host
disease and a co-factor for other virus reactivations. T-lymphocytes play an important role
in the control of virus reactivations. Little is known about the development of
virus-specific T-cells after allogeneic HSCT.
Objective:
The aim of this study was the description of the HHV-6 specific cellular immunity in children
and adolescents after allogeneic HSCT in the context of the clinical course.
Study design and participants:
For this prospective, cross-sectional study, 28 children and adolescents after allogeneic
HSCT who received follow-up support at the respective centers were included. Patients were
enrolled up to 24 months after allogeneic HSCT.. Peripheral venous blood was drawn 3, 6, 9,
12, 18, and 24 months after allogeneic HSCT. Furthermore, a blood sample was taken from 25
age- and sex-matched healthy controls without any inflammatory, immunological, or infectious
diseases. This study was approved by the Institutional Review Board of the Medical University
Graz and patients, parents or legal guardians of patients gave written informed consent in
accordance with the Declaration of Helsinki.
Methods:
3, 6, 9, 12, 18 and 24 months after allogeneic HSCT peripheral blood mononuclear cells were
isolated from patient blood, stimulated with HHV-6-specific antigen (U54) and cultured for 10
days. Furthermore, a blood sample was taken from 25 age- and sex-matched healthy controls
without any inflammatory, immunological, or infectious diseases.
On day 10, peripheral blood mononuclear cells were re-stimulated with the virus antigen U54
for 6 hours and, thereafter, stained for surface markers (CD3, CD4, CD8, CD56) and
intracytoplasmatic activation markers IL-2 (Interleukin-2), IFN-γ (Interferon-γ), TNF-α
(tumor necrosis factor-α) for flow cytometric detection of virus-specific T-cells. T-cells
with intracytoplasmic expression of activation markers after stimulation with the virus
antigen are HHV-6-specific T-cells. This indicated HHV-6 specific cellular immunity.
The virus-specific immunity of patients to HHV-6 was compared to the virus-specific immunity
of children and adolescents of a control group.
