The patients had in common a prior infectious episode, followed by a relatively prolonged period of respiratory insufficiency. They had persistent and nonspecific pulmonary infiltrates of unknown origin, after treatment of their primary disease, which prompted viral culture. The normal PLI observed suggests the involvement of a relatively harmless reactivation of HSV-1, rather than the presence of a primary and damaging infection. Indeed, critically ill patients with sepsis may have late immunodepression, with lymphocytic apoptosis, lymphocytopenia and T-cell anergy, promoting viral reactivation [23, 24] . Apparently, the virus must have been latent in the nerve endings of the mucous membranes of the upper respiratory tract in these patients [2, 15] . Herpesviruses (HSV-1) have frequently been isolated in vivo from respiratory secretions of patients with ARDS [3, 4] and detected in surveillance cultures from the respiratory tract of patients following burns, trauma, transplantation, major surgery and others. However, these viruses are detected in only 3% of lung biopsies from patients with prolonged and unresolving ARDS [3, 7, [9] [10] [11] [12] [13] 15] . The literature is thus widely divergent on the precise role of the virus in pulmonary disease in the critically ill and its contribution to patient morbidity and mortality [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] .