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Low incidence of HHV‐6 reactivation in haploidentical hematopoietic stem cell transplantation with corticosteroid as graft‐vs‐host disease prophylaxis compared with cord blood transplantation

Background Human leukocyte antigen (HLA) mismatch and the administration of immunosuppressive agents are considered risks for human herpesvirus 6 (HHV‐6) reactivation after stem cell transplantation (SCT). However, the incidence of HHV‐6 reactivation in HLA‐mismatched related SCT remains unknown. Me...

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Published in:Transplant infectious disease 2019-06, Vol.21 (3), p.e13073-n/a
Main Authors: Tamaki, Hiroya, Ikegame, Kazuhiro, Yoshihara, Satoshi, Kaida, Katsuji, Yoshihara, Kyoko, Inoue, Takayuki, Kato, Ruri, Nakata, Jun, Fujioka, Tatsuya, Soma, Toshihiro, Okada, Masaya, Ogawa, Hiroyasu
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Language:English
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Summary:Background Human leukocyte antigen (HLA) mismatch and the administration of immunosuppressive agents are considered risks for human herpesvirus 6 (HHV‐6) reactivation after stem cell transplantation (SCT). However, the incidence of HHV‐6 reactivation in HLA‐mismatched related SCT remains unknown. Methods We monitored plasma HHV‐6 DNA loads weekly using real‐time quantitative polymerase chain reaction for 5 weeks after SCT and compared serum IL‐6 levels in HLA‐mismatched SCT groups. Results Compared with detection in all 11 umbilical cord blood transplantation (CBT) patients (100%), plasma HHV‐6 DNA was detected in only 3 of 42 haplo‐SCT patients (7.1%) despite the use of methylprednisolone and antithymocyte globulin as graft‐vs‐host disease prophylaxis and a reduced‐intensity conditioning regimen, respectively. Correspondingly, serum IL‐6 levels in haplo‐SCT patients were significantly lower than those in CBT patients. No HHV‐6‐associated encephalitis developed in either groups. Conclusions Neither HLA disparity nor the use of methylprednisolone and antithymocyte globulin were risk factors for HHV‐6 reactivation in our haplo‐SCT patients. Rather than increasing risk, the administration of immunosuppressive agents potentially prevented HHV‐6 reactivation after haplo‐SCT by suppressing IL‐6 production.
ISSN:1398-2273
1399-3062
DOI:10.1111/tid.13073