Background Community acquired respiratory virus (CARV) infections occur frequently after lung transplantation and may adversely impact outcomes. We hypothesized that while asymptomatic carriage would not increase the risk of chronic lung allograft dysfunction (CLAD) and graft loss, severe infection would. Methods All lung transplant cases between January 2000 and July 2013 performed at our center were reviewed for respiratory viral samples. Each isolation of virus was classified according to clinical level of severity: asymptomatic, symptomatic without pneumonia, and viral pneumonia. Multivariate Cox modeling was employed to assess the impact of CARV isolation on progression to CLAD and graft loss. Results 4408 specimens were collected from 563 total patients with 139 patients producing 324 virus positive specimens in 245 episodes of CARV infection. Overall, the risk of CLAD was elevated by viral infection (HR 1.64, p < 0.01). This risk, however, was due to viral pneumonia alone (HR 3.94, p < 0.01), without significant impact from symptomatic viral infection (HR 0.97, p = 0.94) nor from asymptomatic viral infection (HR 0.99, p = 0.98). The risk of graft loss was not increased by asymptomatic CARV infection (HR 0.74, p = 0.37) nor symptomatic CARV infection (HR 1.39, p = 0.41). Viral pneumonia did, however, significantly increase the risk of graft loss (HR 2.78, p < 0.01). Conclusions With respect to CARV, only viral pneumonia increased the risk of both CLAD and graft loss after lung transplantation. In the absence of pneumonia, respiratory viruses had no impact on measured outcomes.

Our findings validate bronchoalveolar lavage fluid exosomal shuttle RNA as a source for understanding the pathophysiology of AR and for biomarker discovery in lung transplantation.

Staphylococcus aureus is the most commonly isolated gram-positive bacterium after lung transplantation and has been associated with poor post-transplant outcomes, but its effect on BOS and death in the context of the allograft inflammatory environment has not been studied. A three-state Cox semi-Markovian model was used to determine the influence of allograft S. aureus and the ELR+ CXC chemokines on the survival rates and cause-specific hazards for movement from lung transplant (State 1) to BOS (State 2), from transplant (State 1) to death (State 3), and from BOS (State 2) to death (State 3). Acute rejection, pseudomonas pneumonia, BALF CXCL5 and its interaction with S. aureus all increased the likelihood of transition from transplant to BOS. Transition to death from transplant was facilitated by pseudomonas infection and single lung transplant. Movement from BOS to death was affected by the interaction between aspergillus, pseudomonas and CXCL5, but not S. aureus. S. aureus isolation had state specific effects after lung transplantation and only in concert with elevated BALF CXCL5 concentrations did it augment the risk of BOS. Pseudomonas and elevated BALF concentrations of CXCL5 continued as significant risk factors for BOS and death after BOS in lung transplantation.