{'fraction_non_alphanumeric': 0.02119815668202765, 'fraction_numerical': 0.007373271889400922, 'mean_word_length': 5.662576687116564, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Changing virulence of influenza A viruses.

Influenza is a disease characterized by explosive outbreaks, substantial mortality, and enormous morbidity. Much of the reason for its continued prevalence is antigenic variation. Demonstration of a segmented genome (RNA), and elucidation of the phenomenon of genetic reassortment has contributed greatly to our understanding of the mechanism of antigenic variation (1). In contrast to antigenic variation, for many years it has been thought that the clinical manifestations of the disease were constant once acquired; that is, that there were no differences among virus strains in intrinsic virulence (2). We have been studying pulmonary function in young healthy university students since 1974 to obtain data concerning pathogenesis of influenza and to determine the effect of antivirals or viral vaccines on abnormalities in pulmonary function (3-5). The data demonstrate differences among influenza strains with regard to occurrence of alterations in pulmonary resistance, findings which suggest differences in intrinsic viral virulence.