The frequency and complications of respiratory viral infections (RVI) were studied in 50 ambulatory lung transplant patients during a single winter season, using viral antigens, viral cultures and PCR of nasal washes or bronchoalveolar lavages. Patients' survival, episodes of acute rejection and occurrence of bronchiolitis obliterans (BO) or BO syndrome (BOS) were monitored for 1 yr after the study.Overall, 32 (64%) patients had 49 symptomatic episodes. Documented infections included eight due to respiratory syncytial virus (RSV), one due to parainfluenza virus (PIV) and 10 due to influenza (FLU). Four of the FLU infections were serological rises without symptoms. Overall, 17 (34%) patients had documented viral infection; four patients had lower respiratory involvement and two (one RSV, one PIV) were hospitalised for aerosolised ribavirin treatment.After 1 yr there were three (6%) deaths unrelated to RVI. BO or BOS had occurred in one (6%) out of 17 patients with and three (12%) out of 33 without RVI. Respiratory viruses infected onethird of ambulatory lung transplant recipients in a single season.In conclusion, respiratory viral infection was not associated with subsequent graft dysfunction. Larger prospective studies are required to better define the acute and long-term morbidity of these infections.
A reproducible and sensitive rubella plaque neutralization test was established utilizing a Japanese, live, attenuated vaccine strain (KRT‐Kitasato, GMK 4/RT 36/RK 1) in a rabbit kidney cell line (RK‐13). Rubella strain, cell line derivation, addition of complement and temperature of incubation were all critical to the efficiency of plaque formation.
Two hundred sera from 25 children collected longitudinally following rubella vaccination with HPV77DE5 were tested for rubella antibody by three different assays: 1) plaque neutralization, 2) hemagglutination inhibition, and 3) enzyme linked immunoadsorbent assay by commercial kit. Plaque neutralization antibody appeared more slowly after immunization than that determined by hemagglutination inhibition, but persisted in all 22 successfully immunized children over a five to seven year period. The same 22 children had a rise in hemaggulutination inhibition antibody, but lost detectable antibody five to seven years after vaccination. Only 21 children seroconverted by enzyme immunoadsorbent assay. Nine of these lost detectable antibody by five years.
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