Cases reported "Influenza, Human"

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1/3. Intranuclear fibrillary inclusions in influenza pneumonia.

    Electron microscopical study of the lung tissue from a 75-year-old man who died of influenza pneumonia (A/victoria/RI/76) demonstrated fibrillary inclusions in the nuclei of many alveolar lining cells, in bronchial epithelial cells, and also in endothelial cells. These inclusions were morphologically different from those previously reported in experimental animals. In view of previous experimental studies indicating the necessity of nuclear participation in the replication of influenza virus, these inclusions may be virus-induced structures. Also, possibly the presence of these inclusions in the nuclei of many endothelial cells might be indicative of endothelial damage of microvessels and may be a pathogenetically important factor in influenza pneumonia.
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2/3. An influenza A (H1N1) virus, closely related to swine influenza virus, responsible for a fatal case of human influenza.

    In July 1991, an influenza a virus, designated A/maryland/12/91 (A/MD), was isolated from the bronchial secretions of a 27-year-old animal caretaker. He had been admitted to the hospital with bilateral pneumonia and died of acute respiratory distress syndrome 13 days later. Antigenic analyses with postinfection ferret antisera and monoclonal antibodies to recent H1 swine hemagglutinins indicated that the hemagglutinin of this virus was antigenically related to, but distinguishable from, those of other influenza A (H1N1) viruses currently circulating in swine. Oligonucleotide mapping of total viral RNAs revealed differences between A/MD and other contemporary swine viruses. However, partial sequencing of each rna segment of A/MD demonstrated that all segments were related to those of currently circulating swine viruses. sequence analysis of the entire hemagglutinin, nucleoprotein, and matrix genes of A/MD revealed a high level of identity with other contemporary swine viruses. Our studies on A/MD emphasize that H1N1 viruses in pigs obviously continue to cross species barriers and infect humans.
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3/3. Evidence for zanamivir resistance in an immunocompromised child infected with influenza b virus.

    zanamivir, a neuraminidase inhibitor, has shown promise as a drug to control influenza. During prolonged treatment with zanamivir, a mutant virus was isolated from an immunocompromised child infected with influenza b virus. A hemagglutinin mutation (198 Thr-->Ile) reduced the virus affinity for receptors found on susceptible human cells. A mutation in the neuraminidase active site (152 Arg-->Lys) led to a 1000-fold reduction in the enzyme sensitivity to zanamivir. When tested in ferrets, the mutant virus had less virulence than the parent; however, it had a growth preference over the parent in zanamivir-treated animals. Despite these changes, the sensitivity of the mutant virus to zanamivir assessed by a standard test in MDCK cells was unaffected. These data indicate that the current methods for monitoring resistant mutants are potentially flawed because no tissue culture system adequately reflects the receptor specificity of human respiratory tract epithelium.
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