Influenza virus neuraminidase contributes to secondary bacterial pneumonia
Influenza virus neuraminidase contributes to secondary bacterial pneumonia
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DOI：
10.1086/430954
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发表时间：
2005-07-15
影响因子：
6.4
通讯作者：
McCullers, JA
中科院分区：
文献类型：
--
作者：
Peltola, VT;Murti, KG;McCullers, JA
继发性细菌性肺炎是流感流行期间死亡的常见原因。我们假设，病毒特异性因素可能导致年度超额死亡率的差异。从过去50年的代表性菌株中产生并表征了具有神经氨酸酶的重组流感病毒。其神经氨酸酶活性的特定水平与其支持继发性细菌性肺炎的能力相关。具有来自1957年和1997年流感病毒株的神经氨酸酶的重组病毒具有最高水平的活性，而具有来自1968年流感病毒株的神经氨酸酶的病毒具有最低水平的活性。与其他神经氨酸酶相比，来自1957年菌株的神经氨酸酶的高水平活性更有力地支持肺炎链球菌的粘附和小鼠模型中继发性细菌性肺炎的发展。这些数据支持我们的假设，即流感病毒神经氨酸酶有助于继发性细菌性肺炎和随后的过度死亡。
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. Recombinant influenza viruses with neuraminidases from representative strains from the past 50 years were created and characterized. The specific level of their neuraminidase activity correlated with their ability to support secondary bacterial pneumonia. Recombinant viruses with neuraminidases from 1957 and 1997 influenza strains had the highest level of activity, whereas a virus with the neuraminidase from a 1968 strain had the lowest level of activity. The high level of activity of the neuraminidase from the 1957 strain, compared with that of other neuraminidases, more strongly supported the adherence of Streptococcus pneumoniae and the development of secondary bacterial pneumonia in a mouse model. These data lend support to our hypothesis that the influenza virus neuraminidase contributes to secondary bacterial pneumonia and subsequent excess mortality.