In conclusion, the multivirus-chip improvements developed by Ghedin, et al. [2] provide versatile clinical and basic uses. In the near future, such chips are likely to be used to detect viral co-infections in many different clinical settings.  Herpes simplex virus type 1 and normal protein permeability in the lungs of critically ill patients: a case for low pathogenicity? INTRODUCTION: The pathogenicity of late respiratory infections with herpes simplex virus type 1 (HSV-1) in the critically ill is unclear. METHODS: In four critically ill patients with persistent pulmonary infiltrates of unknown origin and isolation of HSV-1 from tracheal aspirate or bronchoalveolar lavage fluid, at 7 (1–11) days after start of mechanical ventilatory support, a pulmonary leak index (PLI) for (67)Gallium ((67)Ga)-transferrin (upper limit of normal 14.1 × 10(-3)/min) was measured. RESULTS: The PLI ranged between 7.5 and 14.0 × 10(-3)/min in the study patients. Two patients received a course of acyclovir and all survived. CONCLUSIONS: The normal capillary permeability observed in the lungs argues against pathogenicity of HSV-1 in the critically ill, and favors that isolation of the virus reflects reactivation in the course of serious illness and immunodepresssion, rather than primary or superimposed infection in the lungs. In some critically ill patients herpes simplex virus (HSV)-1 is isolated from the upper or lower respiratory tract [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] . Immunodepressed patients may be susceptible to transmission and acquisition of viral diseases; alternatively, viral reactivation may occur and may contribute relatively little to morbidity and mortality. Indeed, reactivation of human herpesvirus-6 is common in critically ill patients and does not worsen outcome [16, 17] . In immunocompetent patients, however, isolation of HSV-1 may be associated with viral pneumonia, even if reactivation rather than primary infection is responsible [6, 8, 18] . HSV-1 has been associated with acute respiratory distress syndrome (ARDS) and ventilator-associated pneumonia in the critically ill [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] , as either a primary or a superimposed infection. However, there are few reports of the virus eliciting an infectious host response, as demonstrated by a rise in serum antibodies, by bronchoscopic airway disease, by 'typical' findings on computed tomography of the lungs, or by the presence of giant cells or nuclear inclusion bodies on cytology or biopsy of the lower respiratory tract [3, 5, 9, 10, 18] . Indeed, Tuxen and coworkers [4] observed that prophylactic antiviral therapy in ARDS prevented respiratory HSV-1 emergence but it had no impact on duration of mechanical ventilation or on patient outcome. The pathogenicity of the virus therefore remains unknown, and the rare association in the critically ill of HSV-1 isolation with mortality may represent reactivation of the virus in immunodepressed patients with multiple organ failure and poor outcome [1, 2, 11, 14, 15] , rather than a symptomatic primary infection or superinfection contributing to death.