Our review demonstrates that depending on the methodological assay used and the patient populations studied, CMV infection occurs in 0 to 36% of the critically ill otherwise immunocompetent hosts in the ICU. Among the most frequently studied inciting event for CMV infection in these patients is sepsis [6, 7, 13, 16, 17] . The risk of CMV infection was five-fold higher in patients with sepsis even when controlled for age and the initial severity of illness [10] . In a murine model of CMV infection, cecal ligation and puncture resembling post-surgical intraabdominal sepsis led to reactivation of latent CMV in the lungs and ultimately pulmonary fibrosis [41, 42] . The propensity of sepsis to promote CMV infection may result from its pleiotropic effects on the host immune system. Pro-inflammatory cytokine production such as TNF- and IL-1 in the early phase of sepsis has the potential to activate NF-B and other transcription factors that are key in the reactivation of CMV from latency [43, 44] . The later phase of sepsis, characterized by the generation of immunosuppressive cytokines such as IL-10 and IL-4 is often referred to as compensatory anti-inflammatory response syndrome [45, 46] . Once latent virus is reactivated, these cytokines may further enhance CMV replication. Indeed, in lung transplant recipients, elevated levels of IL-10 in the BAL and/or plasma were associated with delayed CMV clearance [47] . A sustained high level of IL-10 in patients with sepsis has been associated with poor outcomes, presumably due to excessive anti-inflammatory effects [48] .