Risk factors for late cytomegalovirus infection after allogeneic stem cell transplantation using HLA-matched sibling donor: donor lymphocyte infusion and previous history of early CMV infection

Kim, D H; Kim, J G; Lee, N Y; Sung, Woo Jin; Sohn, Sang Kyun; Suh, Jang-Soo; Lee, K S; Lee, K B

doi:10.1038/sj.bmt.1704528

Cited by 19 publications

(8 citation statements)

References 18 publications

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“…CMV reactivation is regarded as a poor prognostic factor for transplant outcomes due to a higher incidence of CMV disease and delayed immune reconstitution after CMV disease, resulting from the use of GCV [12] or the CMV itself [13,14]. In the present study, the incidence of CMV antigenemia was high with early reactivation, yet a low incidence of late CMV reactivation following 100 days after transplantation and CMV disease (7.7%) were observed when compared with historic data on transplant patients without alemtuzumab [15]. The higher incidence of early CMV reactivation and lower incidence of late CMV reactivation would seem to be related to a different pattern of lymphoid recovery.…”

Section: Discussionmentioning

confidence: 44%

Impact of alemtuzumab as conditioning regimen component on transplantation outcomes in case of CMV‐seropositive recipients and donors

et al. 2008

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We studied the incidence of cytomegalovirus (CMV) infection, clinical outcomes, and complications in 39 recipients of alemtuzumab-containing conditioning-stem cell transplantation, who were classified into two groups based on the median dose (35 mg) of alemtuzumab. All the recipients and donors were CMV-seropositive before transplantation. The median survival duration was 321 days (range, 46-1098 days) and the 2-year survival rate was 47.8%. The probability of nonrelapse mortality at 100 days and 2 years was 14.6% and 31.2%, respectively. The cumulative incidence of Grade II-IV acute graft-versus-host disease (GVHD) at Day 100 was 21.8%. The overall incidence of chronic GVHD (cGVHD) was 28.6%, including a 17.9% incidence of extensive cGVHD. The cumulative incidence of CMV antigenemia was 68.0%. There were no statistical differences in the engraftment, acute and cGVHD, relapse, CMV antigenemia, and overall survival (OS) between the two groups. Yet, the nonrelapse mortality (NRM) was significantly lower for the low-dose group (5.9% vs. 51.7%, P 5 0.010). The present study showed that alemtuzumab was effective for GVHD prevention, yet caused a relatively high incidence of CMV antigenemia, regardless of the dose. Thus, a low dose of alemtuzumab (35 mg) would seem to be preferable in an allogeneic SCT setting when both the recipient and the donor are CMV seropositive. Am. J. Hematol. 83:649-653, 2008. V

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Section: Discussionmentioning

confidence: 44%

Impact of alemtuzumab as conditioning regimen component on transplantation outcomes in case of CMV‐seropositive recipients and donors

et al. 2008

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“… 5 Although DLI is an effective treatment approach for both viral infections and viral‐associated diseases, it could possibly increase the risk of GVHD 7 , 8 , 9 and late CMV infection, especially in patients with early CMV infection history. 10 Therefore, unmanipulated DLI administration is limited due to the probability of transferring alloreactive T cells (up to 10% of circulating T cells might be alloreactive) and low levels of antiviral‐specific T cells. 5 Developing new methods in cell isolation, cell culture, and immunodominant epitope prediction has expanded virus‐specific T cell‐based adoptive therapy and facilitated ACT clinical use.…”

Section: Adoptive T Cell Therapymentioning

confidence: 99%

Immunotherapy with adoptive cytomegalovirus‐specific T cells transfer: Summarizing latest gene engineering techniques

Mehdizadeh

Karami

Nazari

et al. 2021

Health Science Reports

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Cytomegalovirus (CMV) infection remains a major complication following allogeneic hematopoietic stem cell transplantation (HSCT). T cell response plays a critical role in inducing long‐term immunity against CMV infection/reactivation that impairs during HSCT. Adoptive T cell therapy (ACT) via transferring CMV‐specific T cells from a seropositive donor to the recipient can accelerate virus‐specific immune reconstitution. ACT, as an alternative approach, can restore protective antiviral T cell immunity in patients. Different manufacturing protocols have been introduced to isolate and expand specific T cells for the ACT clinical setting. Nevertheless, HLA restriction, long‐term manufacturing process, risk of alloreactivity, and CMV seropositive donor availability have limited ACT broad applicability. Genetic engineering has developed new strategies to produce TCR‐modified T cells for diagnosis, prevention, and treatment of infectious disease. In this review, we presented current strategies required for ACT in posttransplant CMV infection. We also introduced novel gene‐modified T cell discoveries in the context of ACT for CMV infection. It seems that these innovations are enabling to improvement and development of ACT utilization to combat posttransplant CMV infection.

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“…The detection of reactivation prior to 100 days post-transplant (Boeckh et al, 2003; Kim et al, 2004; Liu et al, 2015), plasma viral load (Zaia et al, 1997), leukopenia (Jang et al, 2012), lymphopenia (Einsele et al, 1993), and GvHD (Boeckh et al, 2003; Ljungman et al, 2006; Green et al, 2012) represent additional risk factors for HCMV disease. Donor grafts with ≥5 activating killer-cell immunoglobulin-like receptor (KIR) genes or with both KIR2DS2 and KIR2DS4 predict a lower risk of reactivation (Zaia et al, 2009), and the use of donors with multiple or additional activating KIRs is associated with a lower incidence of reactivation (Chen et al, 2006; Cook et al, 2006).…”

Section: Risk Factors For Hcmv Reactivation After Hsctmentioning

confidence: 99%

Human Cytomegalovirus Latency and Reactivation in Allogeneic Hematopoietic Stem Cell Transplant Recipients

et al. 2019

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Human cytomegalovirus (HCMV) reactivation is a major infectious cause of morbidity and mortality after allogeneic hematopoietic stem cell transplantation (HSCT). HCMV is a ubiquitous beta-herpesvirus which asymptomatically infects immunocompetent individuals but establishes lifelong latency, with the potential to reactivate to a life-threatening productive infection when the host immune system is suppressed or compromised. Opportunistic HCMV reactivation is the most common viral complication following engraftment after HSCT and is associated with a marked increase in non-relapse mortality, which appears to be linked to complex effects on post-transplant immune recovery. This minireview explores the cellular sites of HCMV latency and reactivation in HSCT recipients and provides an overview of the risk factors for HCMV reactivation post-HSCT. The impact of HCMV in shaping post-transplant immune reconstitution and its relationship with patient outcomes such as relapse and graft-versus-host disease will be discussed. Finally, we survey current and emerging strategies to prevent and control HCMV reactivation in HSCT recipients, with recent developments including adoptive T cell therapies to accelerate HCMV-specific T cell reconstitution and new anti-HCMV drug therapy for HCMV reactivation after HSCT.

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Risk factors for late cytomegalovirus infection after allogeneic stem cell transplantation using HLA-matched sibling donor: donor lymphocyte infusion and previous history of early CMV infection

Cited by 19 publications

References 18 publications

Impact of alemtuzumab as conditioning regimen component on transplantation outcomes in case of CMV‐seropositive recipients and donors

Impact of alemtuzumab as conditioning regimen component on transplantation outcomes in case of CMV‐seropositive recipients and donors

Immunotherapy with adoptive cytomegalovirus‐specific T cells transfer: Summarizing latest gene engineering techniques

Human Cytomegalovirus Latency and Reactivation in Allogeneic Hematopoietic Stem Cell Transplant Recipients

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