RNA Respiratory Viruses in Solid Organ Transplantation

1. The seasonality of respiratory viral infections among transplant recipients usually follows that of the general population (2,3). 2. The viruses all cause a range of disease, from mild congestion and rhinorrhea to more severe tracheobronchitis, bronchiolitis and pneumonia. No one virus is exclusively associated with one clinical syndrome (i.e. influenza-like illness, croup, etc.). As such, diagnostic strategies should initially be broad, attempting to screen for all recognized viruses (3,4) with particular emphasis on ones that might be amenable to therapy. 3. Transplant recipients often present with mild or atypical symptoms and fever may be absent. Lung transplant recipients, for example, may initially only have subjective symptoms of shortness of breath or subtle changes in pulmonary function testing without more typical symptoms (5). 4. Viral shedding is usually prolonged among transplant recipients. Prolonged shedding is seen even with the use of antivirals and therefore may contribute to the increased risk of resistant variant emergence (1,6). 5. Transplant recipients are at higher risk of infectious complications compared to immunocompetent hosts. Respiratory viral infections are a significant risk factor for subsequent development of fungal and bacterial pneumonia (1). 6. Respiratory viral infections appear to be a risk factor for both acute and chronic rejection with the greatest risk in lung transplant recipients (5,7–9) (II-2), although data on this topic in the literature are conflicting (10). The pathogenesis of the link between respiratory viral infections and rejection is not clearly understood. 7. All pediatric solid organ and lung transplant recipients appear to have the greatest risk of both respiratory viral infections and more severe courses and complications (1). 8. All are potential nosocomial pathogens that can be potentially spread by staff or visitor with mild upper respiratory illness.