We believe that the tracheal aspirates were representative of lower respiratory tract secretions, in the absence of herpes orolabialis and oral epithelial cells in smears for Gram stain of the secretions. Concurrent colonization with other pathogens has previously been described [5, 13] . Because there was no overlap in the duration of stay of the patients, transmission of the virus from one patient to another can be excluded. This further suggests that respiratory HSV-1 infections in the critically ill may result from relatively harmless endogenous reactivation. Although the normal PLI argues against pulmonary parenchymal pathogenicity, tracheobronchitis caused by the virus [18, 25] cannot be ruled out, even in the absence of orolabial lesions, because bronchoscopy was not performed in three of the four patients, even though it was unremarkable in patient 1. The persistent pulmonary infiltrates in our patients may thus relate to slow radiographic resolution of prior bacterial or aspiration pneumonia, rather then superimposed infection. Moreover, computed tomographic images of the lung may be largely nonspecific [26] , and so the precise diagnostic criteria for HSV-1 pneumonia remain unclear. When properly standardized, for instance with respect to cell numbers in bronchoalveolar fluid or tracheal aspirates, quantitative cultures, viral RNA and DNA by polymerase chain reaction, could be helpful together with the PLI in further studies to quantitate viral load and the ratio of replication to shedding, and therefore the pathogenicity of the virus in the lower respiratory tract.