Cellular immunity and active human cytomegalovirus infection in patients with septic shock

J Infect Dis. 2007 Nov 1;196(9):1288-95. doi: 10.1086/522429. Epub 2007 Oct 1.

Abstract

Background: 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.

Methods: Thirty-eight patients with septic shock were monitored, and the 23 CMV-seropositive patients were included in this prospective study.

Results: 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.

Conclusions: 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Cytomegalovirus Infections / complications*
  • Cytomegalovirus Infections / immunology*
  • Female
  • Humans
  • Immunity, Cellular
  • Killer Cells, Natural / physiology
  • Male
  • Middle Aged
  • Shock, Septic / complications*
  • Shock, Septic / immunology*
  • Th1 Cells / physiology
  • Time Factors