Cellular Immunity and Active Human Cytomegalovirus Infection in Patients with Septic Shock

Abstract

Human cytomegalovirus (CMV) is an important opportunistic pathogen after transplantations. In the present study, monitoring of CMV in patients with septic shock was used to discover whether T helper cell type 1 (Th1) cell and natural killer (NK) cell functions interact with CMV reactivation in patients not undergoing immunosuppressive therapy. Thirty-eight patients with septic shock were monitored, and the 23 CMV-seropositive patients were included in this prospective study. Seven patients (30.4%) developed an active CMV infection despite the detection of CMV-reactive Th1 cells. After active CMV infection, the frequency of CMV-reactive Th1 cells increased from a median of 0.52% to 5.04% (P=.009). Active CMV infections were terminated without antiviral therapy within 2 weeks. In parallel, the frequency of staphylococcal enterotoxin B (SEB; superantigen)-reactive Th1 cells increased from a median of 1.11% to 8.48% (P=.027). In patients without active CMV infection, the frequency of CMV-reactive (median, 0.39%) and SEB-reactive (median, 1.11%) Th1 cells did not increase. Cytotoxic NK cell activity was persistently suppressed despite the presence of CD56(+)CD16(+) NK cells. Moreover, interleukin-2 application in vitro did not restore NK cell activity. A proinflammatory immune response may contribute to CMV reactivation in patients with septic shock. Adaptive T cell immunity, more likely than NK cell immunity, may contribute to termination of active CMV infection without antiviral therapy in these patients.