Lower respiratory tract disease caused by respiratory syncytial virus (RSV) is characterized by profound airway mucosa inflammation, both in infants with naturally acquired infection and in experimentally inoculated animal models. The ability to culture influenza was critical in the recognition of the H5N1 avian influenza outbreak in humans in 1997. In most cases, HSV recovery from lower respiratory tract samples of nonimmunocompromised ventilated patients corresponds to viral contamination from the mouth and/or throat but, for some patients, real HSV bronchopneumonitis can develop and it can evolve into ARDS. The “moving wall” represents the time period between the last issue available in JSTOR and the most recently published issue of a journal. Fibroblasts were inspected for cytopathic effect for 7 days. CHAMPLIN and L. Full text Full text is available as a scanned copy of the original print version.
Fresh nasopharyngeal aspirates were inoculated into human diploid fibroblasts and Madin-Darby canine kidney cells and tested for RSV and influenza A virus, respectively, by IPS. Full text Full text is available as a scanned copy of the original print version. Taken together, our results identified Cav-1 as a novel regulator utilized by HSV-1 to evade the host antiviral response mediated by NO production. In addition to the two stricken communities, one apparently unaffected with serious clinical illness and a fourth, in which are located the major hospital and airport in the eastern Arctic, were also studied. One hundred and twenty-four patients were studied serologically and 81 respiratory and other specimens were obtained for virus isolation from 40 of these patients. Clinical records were kept of the outbreak in each area and a detailed questionnaire was filled out for 140 children and their families. Respiratory syncytial virus (RSV) was cultured from eight ill children.
Electron microscopy provided the first evidence of RSV infection. A seroconversion rate of approximately 50% was seen in both affected communities as well as in the clinically unaffected one. The epidemic in the first two communities was characterized by severe pneumonia and frequent hospitalization but no cases of bronchiolitis were seen. No evidence for other causes of this outbreak could be obtained by testing for antibodies to influenza A and B, parainfluenza 1, 2 and 3, adenovirus and herpes simplex viruses. Unusual features of this epidemic of RSV infection include the high attack rate, severe morbidity, illness manifest almost exclusively as pneumonia rather than bronchiolitis and the differences between the expression of disease in different communities. Historical data and clinical observations were inadequate to explain these unusual features.