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Human herpesvirus 6 infection and transient acquired myelodysplasia in children
Sandrine Kagialis-Girard1, Brigitte Durand, Valérie Mialou
1Hematology Laboratory, Hôpital Debrousse, Hospices Civils de Lyon, and Hematology Laboratory, Faculty of Pharmacy, Claude Bernard University, Lyon, France. sandrine.girard@chu-lyon.fr
Insights
Severe human herpesvirus 6 (HHV-6) infection in children can lead to temporary myelodysplastic changes. These findings highlight HHV-6 as a potential cause of dysplasia in myelodysplastic syndrome (MDS) diagnosis.
Area of Science:
- Pediatric Hematology
- Virology
- Oncology
Background:
- Primary human herpesvirus 6 (HHV-6) infection in childhood can present with severe symptoms.
- In some cases, these symptoms mimic myelodysplastic syndromes (MDS).
Purpose of the Study:
- To investigate the link between primary HHV-6 infection and hematopoietic dysplasia in children.
- To determine if HHV-6 infection can cause changes resembling MDS.
Main Methods:
- Evaluation of seven immunocompetent children with cytopenias and bone marrow dysplasia.
- Diagnosis of acute HHV-6 infection confirmed by DNA detection and antibody titers.
- Morphological examination of peripheral blood and bone marrow smears.
Main Results:
- Anemia was the most common cytopenia (5/7 cases).
- Bi- or tri-lineage dysplasia was observed in bone marrow, affecting granulocytic and erythroid cells.
- Myelodysplastic changes were reversible and not due to clonal disorders.
Conclusions:
- Severe HHV-6 infection can induce reversible myelodysplastic changes in children.
- HHV-6 should be considered in the differential diagnosis of dysplasia in children presenting with MDS-like features.
Background:
To demonstrate that primary human herpesvirus 6 (HHV-6) infection in childhood can cause hematopoietic dysplasia that mimics a myelodysplastic syndrome (MDS) in severe cases.
Procedure:
Seven immunocompetent children, who presented at admission with concomitant cytopenias in blood and morphologic features of dysplasia in bone marrow, were evaluated. Diagnosis of acute HHV-6 infection was secondary made by detection of HHV-6 DNA in plasma, bone marrow, or cerebrospinal fluid and measurement of plasma antibody titers. Peripheral blood and bone marrow aspirate smears were examined at diagnosis and during follow-up. Morphologic recognition of myelodysplasia was made according to the recommendations of the Third MIC Cooperative Group.
Results:
Anemia was the most frequent cytopenia (five of seven cases). Bi- or tri-lineage dysplasia was observed in the marrow samples. Granulocytic and erythroid cells were always affected with dysgranulopoiesis and dyserythropoiesis scores equal to or higher than 3. Myelodysplasia was not due to a clonal disorder and disappeared gradually within 1 or 2 months.
Conclusions:
Our results indicate that severe HHV-6 infection may induce reversible myelodysplastic changes. These findings contribute to elucidate the pathogenicity of HHV-6 and furthermore suggest that HHV-6 infection must also be considered as a cause of dysplasia in the differential diagnosis of MDS.
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