Inherited chromosomally integrated human herpesvirus-6 in a patient with XIAP deficiency.
XIAP deficiency
chromosomal integration
hematopoietic cell transplantation
hemophagocytic lymphohistiocytosis
human herpesvirus 6
Journal
Transplant infectious disease : an official journal of the Transplantation Society
ISSN: 1399-3062
Titre abrégé: Transpl Infect Dis
Pays: Denmark
ID NLM: 100883688
Informations de publication
Date de publication:
Oct 2020
Oct 2020
Historique:
received:
31
03
2020
accepted:
12
05
2020
pubmed:
20
5
2020
medline:
4
8
2021
entrez:
20
5
2020
Statut:
ppublish
Résumé
Human herpesvirus-6 (HHV-6) is a common pathogen affecting the human population. Primary HHV-6 infection generally occurs during infancy and causes exanthema subitum. Moreover, HHV-6 may exhibit inherited chromosomally integrated HHV-6 (iciHHV-6) in certain individuals. Although iciHHV-6 is generally known to be nonpathogenic, it may cause reactivation in patients with primary immunodeficiency disease (PID). XIAP deficiency is a rare PID characterized by recurrent hemophagocytic lymphohistiocytosis (HLH). It has been reported that the Epstein-Barr virus primarily causes HLH; however, the other pathogens, including HHV-6, can also cause this complication. We encountered a case of XIAP deficiency accompanied by iciHHV-6. He suffered from recurrent HLH, for which allogeneic bone marrow transplantation (BMT) was performed as a curative therapy. During the course of BMT, the patient experienced HLH three times, but there was no reactivation of endogenous HHV-6 from iciHHV-6. Finally, the patient achieved complete donor chimerism and a decline in HHV-6 DNA copy number in whole blood. This case report demonstrates no evidence of reactivation of iciHHV-6 during BMT in a patient with XIAP deficiency.
Substances chimiques
X-Linked Inhibitor of Apoptosis Protein
0
XIAP protein, human
0
Types de publication
Case Reports
Langues
eng
Sous-ensembles de citation
IM
Pagination
e13331Subventions
Organisme : MEXT/ JSPS KAKENHI
ID : Grant Number JP17K10099
Informations de copyright
© 2020 Wiley Periodicals LLC.
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