Differential onset of apoptosis in influenza A virus H5N1- and H1N1-infected human blood macrophages
Differential onset of apoptosis in influenza A virus H5N1- and H1N1-infected human blood macrophages
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DOI：
10.1099/vir.0.82423-0
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发表时间：
2007-04-01
影响因子：
3.8
通讯作者：
Lau, Allan S. Y.
中科院分区：
文献类型：
--
作者：
Mok, Chris K. P.;Lee, Davy C. W.;Lau, Allan S. Y.
高致病性禽流感病毒A/Hong Kong/483/97(H5N1/97)的发病机制仍有待调查。最近的研究表明，H5N1对人巨噬细胞促炎细胞因子的调节失调是一个依赖p38蛋白的过程。结果表明，巨噬细胞可能在疾病的严重程度中起作用。为了进一步研究H5N1感染后的细胞反应，我们研究了原代血巨噬细胞的凋亡及其相关途径。在这里，它表明，H5N1/97病毒触发了感染的巨噬细胞的凋亡，包括caspase和PARP的激活，与H1N1病毒相比，起病延迟。在感染H5N1/97病毒前体的人巨噬细胞中也发现了类似的结果。因此，这些结果表明，H5N1/97及其相关前体亚型感染的巨噬细胞发生凋亡的延迟可能是病原体在细胞内存活时间更长的一种手段，这可能是H5N1疾病在人类发病机制中的一部分。
Pathogenesis of the highly pathogenic avian influenza virus A/Hong Kong/483/97 (H5N1/97) remains to be investigated. It was demonstrated recently that H5N1 dysregulation of proinflammatory cytokines in human macrophages is a p38-kinase-dependent process. The results indicated that macrophages may play a role in disease severity. To investigate cellular responses to H5N1 infection further, apoptosis and its related pathways were studied in primary blood macrophages. Here, it is shown that the H5N1/97 virus triggered apoptosis, including caspases and PARP activation, in infected macrophages with a delayed onset compared with H1N1 counterparts. Similar results were also found in human macrophages infected by precursors of the H5N1/97 virus. Thus, these results showed that the delay in apoptosis onset in macrophages infected by H5N1/97 and its related precursor subtypes may be a means for the pathogens to have longer survival in the cells; this may contribute to the pathogenesis of H5N1 disease in humans.