Birgitta Versluijs

55 Association between respiratory virus and alloimmune lung syndromes A remark about the definition of IPS is warranted. In the consensus definition of IPS (established by a 1997 National Institutes of Health workshop), all infectious agents, including RVs, should be excluded. In our patients, we observed prolonged shedding of RV for months, and thus we could not formally diagnose IPS. In all patients, the initial URTI symptoms disappeared spontaneously within 1-2 weeks, however. Subsequently, after a period of at least 14 days without significant respiratory problems, symptoms of hypoxia and/or airway obstruction recurred. We believe that this represents not a direct progression of viral infection, but rather a combination of several factors in which allo- reactivity (triggered by tissue damage because of persistent viral infection) plays a pivotal role. Therefore, we chose to define IPS as discussed earlier, not taking into account the presence of an RV identified by PCR as was done in this study. Moreover, the formal definition of IPS was promulgated in an era when molecular diagnosis of RV was not yet available. We hypothesize that RVs may contribute to the pathogenesis of any allo-LS as follows. The RV damages the respiratory epithelium, causing an inflammatory response at the time of immune recovery. Normally IPS and BOS/BOOP are viewed as distinct clinical entities, and so we first studied them separately. Because we noted the same strong as- sociations among RV positivity, GVHD, and OS in the 2 groups, we combined both IPS and BOS/BOOP in subsequent analyses. We also combined BM and PBSC sources in our analysis. It would be interesting to evaluate patients receiving PBSCs as a separate group, because of their apparent higher risk of chronic GVHD (cGVHD). The small number of patients our cohort who received PBSCs (n = 7) precludes meaningful analysis, however. Numerous studies have explored the incidence and outcome of both nosocomial and community-acquired RV infections after HSCT. 7-16 Reported incidence varies from 1% to 56%. This wide range of incidence can be explained by differences among studies in the definition of RV infection, the period of monitoring for RV infection (eg, inpatients/ outpatients, seasonal influence), and sensitivity of the analysis methods used. In our co- hort, the high incidence of RV URTI (50%) might be attributed to our close monitoring for respiratory symptoms and performance of RT-PCR surveillance assays. In addition, nosocomial RV infections were frequently observed, and genotyping studies suggested that these had spread throughout the ward during the study period, also contributing to the relatively high incidence (data not shown). Literature data on the morbidity associated with RV infection after HSCT are conflicting. Some groups found no progression of viral URTI to LRTI in patients after HSCT, 10,15 whereas others reported progression in up to 58% of patients. 7,8,11,13,16 In our cohort, we found no direct progression to LRTI. Almost all patients had mild URTI symptoms and recovered spontaneously. The median day of onset of RV infection was only 16 days in 3