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Kinetics of interferon‐gamma producing cytomegalovirus (CMV)‐specific CD4+ and CD8+ T lymphocytes and the risk of subsequent CMV viremia after allogeneic hematopoietic stem cell transplantation
Author(s) -
Eid A.J.,
Brown R.A.,
Hogan W.J.,
Lahr B.D.,
EckelPassow J.E.,
Litzow M.R.,
Razonable R.R.
Publication year - 2009
Publication title -
transplant infectious disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.69
H-Index - 67
eISSN - 1399-3062
pISSN - 1398-2273
DOI - 10.1111/j.1399-3062.2009.00446.x
Subject(s) - viremia , medicine , cytomegalovirus , cd8 , hematopoietic stem cell transplantation , immunology , transplantation , virology , interferon gamma , human immunodeficiency virus (hiv) , immune system , herpesviridae , viral disease
Background. Deficiencies in cytomegalovirus (CMV)‐specific T lymphocytes impair the immunologic response against CMV reactivation after allogeneic hematopoietic stem cell transplantation (HSCT). Methods. A time‐dependent analysis was conducted to determine the association between the percentages and kinetics of interferon‐gamma‐producing CMV‐specific CD4+ and CD8+ T lymphocytes and CMV viremia among 30 allogeneic HSCT recipients. Results. Higher percentages of CD4+ T lymphocytes activated with CMVpp65 (hazard ratio [HR]: 2.06; 95% confidence interval [95% CI]: 1.18–3.6; P =0.011) and CMV lysate (HR: 1.18; 95% CI: 0.99–1.42; P =0.072), and higher percentages of CD8+ T lymphocytes activated by CMV immediate early‐1 (HR: 1.2; 95% CI: 1.01–1.43; P =0.038) and CMVpp65 (HR: 1.12; 95% CI: 1.0–1.27; P =0.060) were associated with time‐to‐CMV viremia. Furthermore, a higher degree in the decline of CMV lysate‐activated CD4+ T lymphocytes (HR: 1.14; 95% CI: 0.96–1.36; P =0.125) and CMVpp65‐activated CD8+ T lymphocytes (HR: 1.36; 95% CI: 1.03–1.78; P =0.031) was suggestive of or significantly associated with time‐to‐CMV viremia. Conclusions. Higher levels of CMV‐specific CD4+ and CD8+ T lymphocytes were associated with subsequent CMV viremia after HSCT. The association between CMV viremia and the degree of decline in CMV‐specific T lymphocytes suggests that severe disruption in homeostatic CMV‐specific immune environment contributes to the immunopathogenesis of CMV after allogeneic HSCT.