Cytomegalovirus (CMV) is a human herpes virus known to infect more than 50-90% of US adults and is known to be a major cause of morbidity and mortality in immunocompromised patients. CMV infection can be acquired through multiple means, including: mother-to-child (in utero, breast milk), infected body fluids (saliva, genital secretions), blood transfusion or organ transplant. The prevalence of CMV infection increases with age throughout life such that by age 90, ~90% of persons will have acquired CMV infection. In immunocompetent persons, following primary infection by any of the routes noted above, CMV is controlled by the immune system and establishes latency ("dormancy") in multiple organs/cell-types for the life of the host. In particular, the lung represents one of the largest reservoirs of latent CMV in seropositive hosts, and may explain the propensity for CMV-associated pulmonary disease in predisposed hosts. During periods of immunosuppression (or as a result of specific stimuli such as TNF-α, LPS, or catecholamines that are commonly associated with critical illness & sepsis [CMV can reactivate from latency (preferentially in the lung) to produce active infection (viral replication). In persons with impaired cellular immunity, reactivation can progress to high-grade CMV replication and commonly leads to tissue injury and clinically-evident disease such as CMV pneumonia. Lower-grade CMV reactivation that is otherwise clinically silent ("subclinical") can also be detected in apparently immunocompetent persons with critical illness using sensitive techniques such as PCR. In addition, even low-level, otherwise asymptomatic subclinical CMV reactivation can produce significant biologic effects both in vitro and in vivo, such as inflammation, fibrosis and immunosuppression. Each of these biologic effects of subclinical CMV infection has either previously been demonstrated (inflammation, fibrosis) or could theoretically be important (immunosuppression) in sepsis-associated ALI and its complications. These biological effects of CMV have been shown to occur through various mediators and other indirect means [Importantly, several important CMV-associated adverse clinical outcomes in transplant populations [allograft rejection, secondary infections] are not necessarily accompanied by overt CMV disease and can only be detected by relatively sensitive means of virus detection such as PCR.