Common Cold Virus Leads To Death In Lung Transplant Patients

The research appears in the second issue for December 2006 of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.

Laurent Kaiser, M.D., of the Central Laboratory of Virology at the University Hospital of Geneva, Switzerland, and 13 associates assessed the incidence of chronic rhinovirus infection and its potential clinical impact on 69 lung transplant recipients at two centers. Over a 19-month period, they screened all lung transplant patients using molecular analysis to detect 13 different respiratory viruses.

Human rhinovirus is a leading cause of respiratory infections in adults and children. Adults, on average, get infected with the virus once per year. Lung transplant patients, with impaired immune systems due to drugs to halt rejection, are at potentially higher risk from the virus.

"Our evidence demonstrates that rhinoviral disease is not exclusively limited to the upper respiratory tract," said Dr. Kaiser. "It can also lead to lower respiratory complications, which immunosuppressed patients can be at higher risk of developing."

Although eight lung transplant patients had transient rhinoviral infections, three showed a persistent infection. The others were able to clear the virus from their system.

"We confirmed the persistence of a single strain in each of three lung transplant recipients clinically infected by rhinovirus," said Dr. Kaiser. "Two of the three had chronic upper respiratory tract infections. All three had relapsing 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."