Influence of major histocompatibility complex class I chain-related gene A polymorphisms on cytomegalovirus disease after allogeneic hematopoietic cell transplantation.


Journal

Hematology/oncology and stem cell therapy
ISSN: 2589-0646
Titre abrégé: Hematol Oncol Stem Cell Ther
Pays: Saudi Arabia
ID NLM: 101468532

Informations de publication

Date de publication:
Mar 2020
Historique:
received: 20 02 2019
revised: 18 09 2019
accepted: 27 10 2019
pubmed: 28 12 2019
medline: 8 10 2020
entrez: 28 12 2019
Statut: ppublish

Résumé

Cytomegalovirus (CMV) infection and disease are common infectious complications after allogeneic hematopoietic cell transplantation (alloHCT). Major histocompatibility complex (MHC) class I chain-related gene A (MICA) is a ligand of the natural killer (NKG2D) receptor on immune effector cells that helps mediate NK cell alloreactivity. We hypothesized that MICA polymorphisms may influence CMV infection and disease incidence after alloHCT. We conducted a retrospective analysis of 423 adults at the Cleveland Clinic with hematologic malignancies treated with a matched related or unrelated donor alloHCT. CMV cases analyzed included a compositive of instances of viral copy replication above detection limits as well as any biopsy-proven tissue invasive disease episodes. Genotypes at the MICA-129 position have been categorized as weak (valine/valine; V/V), intermediate (methionine/valine; M/V), or strong (methionine/methionine; M/M) receptor affinity. In multivariable analysis, V/V donor MICA-129 genotype was associated with CMV infection and disease (hazard ratio [HR] = 1.40; 95% confidence interval [CI], 1.00-1.96; p = .05), but not MICA mismatch (HR = 1.38; 95% CI, 0.83-2.29; p = .22). There was no association of acute or chronic GVHD with MICA donor-recipient mismatch (HR = 1.05; 95% 95% CI, 0.66-1.68; p = .83 and HR = 0.94; 95% CI, 0.51-1.76; p = .85, respectively) or V/V donor MICA-129 genotypes (HR = 1.02; 95% CI, 0.79-1.31; p = .89 and HR = 0.89; 95% CI, 0.65-1.22; p = .47, respectively). These findings suggest that the donor MICA-129 V/V genotype with weak NKG2D receptor binding affinity is associated with an increased risk of CMV infection and disease after alloHCT.

Sections du résumé

OBJECTIVE/BACKGROUND OBJECTIVE
Cytomegalovirus (CMV) infection and disease are common infectious complications after allogeneic hematopoietic cell transplantation (alloHCT). Major histocompatibility complex (MHC) class I chain-related gene A (MICA) is a ligand of the natural killer (NKG2D) receptor on immune effector cells that helps mediate NK cell alloreactivity. We hypothesized that MICA polymorphisms may influence CMV infection and disease incidence after alloHCT.
METHODS METHODS
We conducted a retrospective analysis of 423 adults at the Cleveland Clinic with hematologic malignancies treated with a matched related or unrelated donor alloHCT. CMV cases analyzed included a compositive of instances of viral copy replication above detection limits as well as any biopsy-proven tissue invasive disease episodes. Genotypes at the MICA-129 position have been categorized as weak (valine/valine; V/V), intermediate (methionine/valine; M/V), or strong (methionine/methionine; M/M) receptor affinity.
RESULTS RESULTS
In multivariable analysis, V/V donor MICA-129 genotype was associated with CMV infection and disease (hazard ratio [HR] = 1.40; 95% confidence interval [CI], 1.00-1.96; p = .05), but not MICA mismatch (HR = 1.38; 95% CI, 0.83-2.29; p = .22). There was no association of acute or chronic GVHD with MICA donor-recipient mismatch (HR = 1.05; 95% 95% CI, 0.66-1.68; p = .83 and HR = 0.94; 95% CI, 0.51-1.76; p = .85, respectively) or V/V donor MICA-129 genotypes (HR = 1.02; 95% CI, 0.79-1.31; p = .89 and HR = 0.89; 95% CI, 0.65-1.22; p = .47, respectively).
CONCLUSION CONCLUSIONS
These findings suggest that the donor MICA-129 V/V genotype with weak NKG2D receptor binding affinity is associated with an increased risk of CMV infection and disease after alloHCT.

Identifiants

pubmed: 31881183
pii: S1658-3876(19)30104-9
doi: 10.1016/j.hemonc.2019.10.001
pii:
doi:

Substances chimiques

H-2 Antigens 0
H-2K(K) antigen 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

32-39

Informations de copyright

Copyright © 2019 King Faisal Specialist Hospital & Research Centre. Published by Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest There are no conflicts of interest to report.

Auteurs

Sagar S Patel (SS)

Blood and Marrow Transplant Program, Division of Hematology and Hematologic Malignancies, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT, USA.

Lisa A Rybicki (LA)

Quantitative Health Sciences, Cleveland Clinic, Cleveland, OH, USA.

Melissa Yurch (M)

Blood and Marrow Transplant Program, Department of Hematology and Medical Oncology, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.

Dawn Thomas (D)

Allogen Laboratories, Cleveland Clinic, Cleveland, OH, USA.

Hien Liu (H)

Department of Blood and Marrow Transplant and Cellular Immunotherapy, Moffitt Cancer Center, Tampa Bay, FL, USA.

Robert Dean (R)

Blood and Marrow Transplant Program, Department of Hematology and Medical Oncology, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.

Deepa Jagadeesh (D)

Blood and Marrow Transplant Program, Department of Hematology and Medical Oncology, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.

Brian Hill (B)

Blood and Marrow Transplant Program, Department of Hematology and Medical Oncology, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.

Brad Pohlman (B)

Blood and Marrow Transplant Program, Department of Hematology and Medical Oncology, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.

Brian Bolwell (B)

Blood and Marrow Transplant Program, Department of Hematology and Medical Oncology, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.

Rabi Hanna (R)

Pediatric Blood and Marrow Transplant Program, Pediatrics Institute and Children's Hospital, Cleveland Clinic, Cleveland, OH, USA.

Betty K Hamilton (BK)

Blood and Marrow Transplant Program, Department of Hematology and Medical Oncology, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.

Matt Kalaycio (M)

Blood and Marrow Transplant Program, Department of Hematology and Medical Oncology, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.

Aaron T Gerds (AT)

Blood and Marrow Transplant Program, Department of Hematology and Medical Oncology, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.

Eric Cober (E)

Department of Infectious Disease, Respiratory Institute, Cleveland Clinic, Cleveland, OH, USA.

Sherif Mossad (S)

Department of Infectious Disease, Respiratory Institute, Cleveland Clinic, Cleveland, OH, USA.

Aiwen Zhang (A)

Pathology and Laboratory Medicine Institute, Cleveland Clinic, Cleveland, OH, USA.

Navneet S Majhail (NS)

Blood and Marrow Transplant Program, Department of Hematology and Medical Oncology, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.

Medhat Askar (M)

Department of Pathology, Baylor University Medical Center, Dallas, TX, USA.

Ronald Sobecks (R)

Blood and Marrow Transplant Program, Department of Hematology and Medical Oncology, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: sobeckr@ccf.org.

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