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The influenza virus neuraminidase contributes to secondary bacterial pneumonia

机译:流感病毒神经氨酸酶导致继发性细菌性肺炎

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摘要

Secondary bacterial pneumonia is a common cause of death during influenza epidemics. We hypothesized that virus-specific factors could contribute to differences in annual excess mortality. A set of recombinant viruses with neuraminidases from representative influenza virus strains from the last 50 years was created and characterized. Their specific neuraminidase activities correlated with their ability to support secondary bacterial infections. Recombinant viruses with the 1957 and 1997 neuraminidases had the highest activities, while a virus with the 1968 neuraminidase had the lowest activity. The high activity of the 1957 neuraminidase, when compared to other neuraminidases, more strongly supported bacterial adherence in vitro and secondary pneumococcal pneumonia in a mouse model. These data lend support to our hypothesis that the neuraminidase of influenza viruses contributes to secondary bacterial infections and subsequent excess mortality.
机译:继发性细菌性肺炎是流感流行期间常见的死亡原因。我们假设病毒特异性因素可能会导致每年超额死亡率的差异。创建并表征了一组具有近50年代表性流感病毒株的神经氨酸酶的重组病毒。它们的特定神经氨酸酶活性与其支持继发细菌感染的能力有关。具有1957年和1997年神经氨酸酶的重组病毒具有最高的活性,而具有1968年神经氨酸酶的病毒具有最低的活性。与其他神经氨酸酶相比,1957年神经氨酸酶的高活性在小鼠模型中更强烈地支持了细菌的体外粘附和继发性肺炎球菌性肺炎。这些数据支持了我们的假设,即流感病毒的神经氨酸酶会导致继发性细菌感染和随后的过度死亡。

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