Persistent lack of human herpesvirus-6 specific T-helper cell response in liver transplant recipients

: Background. Specific immunologic defects predisposing to human herpesvirus‐6 (HHV‐6), e.g. the role of HHV‐6 specific T‐helper cell memory response in liver transplant recipients, have not been assessed. Methods. T‐helper function (mitogen ConA response) as a marker of overall immunocompetence and T‐helper response (memory response) specific to HHV‐6 and cytomegalovirus (CMV) were assessed in 15 liver transplant recipients and compared with 25 healthy subjects. Samples were tested pretransplant, at 2 weeks, 1 month, 2–3 months, and 1 year posttransplantation. Stimulation index (SI) >3 was considered a positive response. Results. Seven percent (1/15) of the transplant recipients at any time posttransplantation, as compared to 64% (16/25) of the healthy subjects, had a positive HHV‐6 memory response (P = 0.00065). HHV‐6‐specific memory response in transplant recipients at 2 weeks (SI 1.43), 1 month (SI 1.1), and 2–3 months (SI 1.3) was significantly more suppressed than in healthy subjects (SI 17.5, P = 0.0001). Although transplant recipients as compared to healthy subjects also had a lower CMV‐specific memory response posttransplant (P = 0.0439), CMV‐specific memory response recovered significantly at 1 month (P = 0.03) and at 2–3 months (P = 0.027) as compared to that at 2 weeks. However, HHV‐6 memory response was persistently absent up to 2–3 months with partial recovery at 1 year; 7% of the patients at 2–3 months, but 25% at 1 year had a positive HHV‐6 specific memory response. Forty percent (6/15) of the patients developed HHV‐6 viremia a mean of 4 weeks posttransplant. Patients with HHV‐6 viremia had greater suppression of HHV‐6 memory response at 1 month than those without viremia (mean SI, 0.96 vs. 1.3, P = 0.08). All but one of the patients had a positive ConA response. Conclusion. Prolonged suppression of HHV‐6 memory response, but not overall T‐helper cell function was documented and may play a role in the pathogenesis of HHV‐6 infection in liver transplant recipients. Memory response to CMV after liver transplantation was significantly more robust than to HHV‐6.