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Transient erythroblastopenia of childhood associated with human herpesvirus type 6, variant B
1Department of Pathology, University of Pittsburgh, Pennsylvania, USA.
Insights
Human herpesvirus type 6 (HHV-6) DNA was detected in children with transient erythroblastopenia of childhood (TEC). This suggests HHV-6 may cause TEC in young children.
Area of Science:
- Pediatric Hematology
- Virology
- Immunology
Background:
- Transient erythroblastopenia of childhood (TEC) is a hematologic disorder in young children (3 months to 4 years) characterized by anemia and reticulocytopenia.
- A viral etiology for TEC has been previously suspected but not confirmed.
- Bone marrow aspirate (BMA) analysis in TEC typically shows decreased red blood cell precursors.
Observation:
- This study analyzed bone marrow aspirate-derived DNA from 14 children with hematologic disorders, including two with TEC, for human herpesvirus type 6 (HHV-6) and human parvovirus B19 DNA.
- Polymerase chain reaction testing identified HHV-6 variant B DNA in both TEC patients.
- The BMAs from these TEC patients exhibited large pronormoblasts and significant lymphoid infiltration.
Findings:
- HHV-6 variant B DNA was exclusively detected in children diagnosed with TEC.
- No HHV-6 or parvovirus B19 DNA was found in the non-TEC patients analyzed.
- The presence of HHV-6 DNA in TEC patients suggests a potential causative link.
Implications:
- The findings propose that HHV-6 may be a causative agent of TEC in immunocompetent children.
- This hypothesis is supported by HHV-6's known in vitro and in vivo effects on hematopoietic progenitor cells (BFU-E and GM-CFU).
- Further research is warranted to elucidate the precise mechanism of HHV-6-induced TEC.
Abstract:
Transient erythroblastopenia of childhood (TEC) is a disorder of young children ages 3 months to 4 years that is characterized by anemia associated with reticulOcytopenia and decreased red blood cell precursors in the bone marrow aspirate (BMA). A viral cause has been suspected for TEC. Bone marrow aspirate-derived DNA from 14 children with anemia or another hematologic disorder, including two children with TEC, were analyzed by polymerase chain reaction for human herpesvirus type 6 (HHV-6) DNA and human parvovirus B19 DNA. Testing revealed an HHV-6 variant B DNA in both children with TEC but not in the children who did not have TEC. The BMAs from these two children contained large pronormoblasts and an extensive lymphoid infiltrate. We proposed that HHV-6 may be a causative agent of TEC in immunocompetent children. This hypothesis is based on the demonstrated ability of HHV-6 to suppress the formation of burst-forming units-erythroid (BFU-E) and granulocyte macrophage-colony-forming units (GM-CFU) in vitro, and in vivo in HHV-6-infected patients who undergo bone marrow transplantation.