Abstract
Approximately 75% of cord blood transplant (CBT) recipients experience human herpes virus-6 (HHV-6) reactivation. Considering the immunomodulatory effects of HHV-6, we hypothesized that early HHV-6 reactivation may influence the risk of relapse of the underlying hematologic malignancy. In 152 CBT recipients with hematological malignancies, we determined the association between HHV-6 reactivation by day +28 and 2-year cumulative incidence of relapse. In univariate analysis, the absence of HHV-6 reactivation (n = 32) was associated with less relapse (26 [18-35]% vs. 7 [0-17]% in groups with vs. without HHV-6 reactivation, respectively; P =.03). This difference was due to a remarkably low relapse incidence among patients without HHV-6 reactivation. In multivariable analysis, the absence of HHV-6 reactivation was associated with less relapse (hazard ratio [95% confidence interval]: 0.2 [0.05-0.9], P =.03). This association was independent of patient-, disease-, and transplant-related characteristics known to influence the risk of relapse. Natural killer cell and T-cell reconstitution at day +28 were similar between patients with vs. without HHV-6 reactivation. Our results suggest that CB allografts not complicated by HHV-6 reactivation by day +28 have a powerful graft-versus-tumor effect. Knowledge about early HHV-6 reactivation may stratify patients at day +28 into low vs. high relapse risk groups.
Original language | English (US) |
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Pages (from-to) | 1014-1019 |
Number of pages | 6 |
Journal | American Journal of Hematology |
Volume | 93 |
Issue number | 8 |
DOIs | |
State | Published - Aug 2018 |
Bibliographical note
Funding Information:Research reported in this publication was supported by NIH grant P30 CA77598 utilizing the Biostatistics and Bioinformatics Core and the Bio-specimen Repository in the Translational Therapy Laboratory shared resource of the Masonic Cancer Center, University of Minnesota and by the National Center for Advancing Translational Sciences of the NIH award UL1TR000114. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. JSM and DJW were supported by NIH grant P01 CA111412, and JSM and CGB by NIH grant P01 CA65493.
Funding Information:
Research reported in this publication was supported by NIH grant P30 CA77598 utilizing the Biostatistics and Bioinformatics Core and the Biospecimen Repository in the Translational Therapy Laboratory shared resource of the Masonic Cancer Center, University of Minnesota and by the National Center for Advancing Translational Sciences of the NIH award UL1TR000114. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. JSM and DJW were supported by NIH grant P01 CA111412, and JSM and CGB by NIH grant P01 CA65493.
Publisher Copyright:
© 2018 Wiley Periodicals, Inc.