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Common cold virus leads to death in lung transplant patients

lower respiratory infections, and two subsequently died with graft dysfunction."

Dr. Kaiser noted that the persistent infection suggests that certain cases can act as viral reservoirs to sustain transmission of rhinovirus.

"Therefore, in lung transplant recipients with severe immunosuppression, clinical rhinovirus infection needs to be considered," said Dr. Kaiser. "This point might have substantial implications in terms of diagnostic procedures, clinical management, and anti-viral use, if available."

In an editorial on the research in the same issue of the journal, Marc B. Hershenson, M.D., of the University of Michigan, Ann Arbor, and Sebastian L. Johnston, M.D., Ph.D., of the National Heart and Lung Institute at Imperial College in London, wrote: "The report by Drs. Kaiser and colleagues ends once and for all the argument that rhinovirus cannot infect the lower airways. Although interesting new data suggest that rhinoviruses may induce proinflammatory responses in lung cells independent of viral replication, replication is almost certainly required for a maximal response. However, until the present report, which includes positive bronchoalveolar cultures and lung immunochemistry, incontrovertible evidence of rhinoviral replication in the lung in the setting of spontaneous infection has been lacking. This report informs our understanding of the mechanisms underlying rhinovirus-induced exacerbations of asthma and COPD."

They continued: "These exciting new data raise the possibility that patients with asthma and other patients with chronic airway disease are unusually susceptible to rhinovirus infection leading to increased rates of exacerbation. These results may also help explained the increased susceptibility of children to rhinovirus infections. Further studies on susceptibility to rhinovirus infection in the population are now required."
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Source:American Thoracic Society


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