RNA respiratory viral infections in solid organ transplant recipients

A wide range of RNA respiratory viruses have been identi-ﬁedascausesofsigniﬁcantmorbidityandmortalityamongtransplant recipients, including inﬂuenza, respiratory syn-cytial virus (RSV), parainﬂuenza virus (PIV), rhinovirus, hu-manmetapneumovirus(hMPV),coronavirus,bocavirusandpolyomaviruses (1) (Table 1). Several features are commonamong all of these viruses in the transplant population:1. The seasonality of respiratory viral infections amongtransplant recipients usually follows that of the generalpopulation (2,3).2. The viruses all cause a range of disease, from mild con-gestion and rhinorrhea to more severe tracheobronchi-tis, bronchiolitis and pneumonia. No one virus is ex-clusively associated with one clinical syndrome (i.e.inﬂuenza-like illness, croup, etc.). As such, diagnosticstrategiesshouldinitiallybebroad,attemptingtoscreenfor all recognized viruses (3,4) with particular emphasison ones that might be amenable to therapy. Symptomscommonly associated with a respiratory viral infectioninclude fevers, nasal congestion, rhinorrhea, wateryeyes, cough, sore throat, sputum production, wheez-ing, shortness of breath and fevers.3. Transplant recipients often present with mild or atypi-cal symptoms. Lung transplant recipients, for example,may initially only have subjective symptoms of short-ness of breath or subtle changes in pulmonary functiontesting without more typical symptoms (5). Fever maybe absent in transplant recipients with pneumonia ormay be the sole presenting sign or symptom (1,4). Assuch, any fever or respiratory symptom should promptthe consideration of a respiratory viral infection as thepotential cause.4. Viral shedding is usually prolonged among transplantrecipients. Prolonged shedding is seen even with theuse of antivirals and therefore may contribute to theincreased risk of resistant variant emergence (1,6).5. Transplant recipients are at higher risk of infectiouscomplications compared to immunocompetent hosts.In the older studies, initial evidence of or progressionto lower tract involvement with viruses occurred fre-quently, but may in part be due to ascertainment biasesas sicker patients were more likely to be seen by physi-cians and have specimens sent for viral assays (1). Res-piratory viral infections are a signiﬁcant risk factor forsubsequent development of fungal and bacterial pneu-monia (1). Other infections, such as CMV viremia, maycomplicate respiratory viral infections as well.6. Respiratory viral infections appear to be a risk factor forboth acute and chronic rejection with the greatest riskin lung transplant recipients (5,7–9) (II-2). Concurrentrejection and graft dysfunction has been documentedwith other solid organ transplant recipients as well, al-though at a lower frequency than in lung transplant re-cipients (1) (III). The pathogenesis of the link betweenrespiratory viral infections and rejection is not clearlyunderstood.7. All pediatric solid organ and lung transplant recipientsappear to have the greatest risk of both RNA viral in-fections and more severe courses and complications(1).8. All are potential nosocomial pathogens which can bepotentially spread by staff or visitor with mild upperrespiratory illness.9. There are few prospective studies of respiratory virusinfections in most solid organ transplant populations,withtheexceptionoflungtransplantrecipients.Mostofthese studies were retrospective in nature and focusedonindividualswhowerehospitalizedwithinfections(1).Inaddition,moststudiesevaluatedpatientsclosetothetime of transplantation when specimens were morelikely to be obtained for diagnosis. This likely leads toan overestimation of the severity and underestimationof the incidence of these infections among transplantrecipients.