目的探索含a-Arrestin结构域蛋白3(a-Arrestin-domain-containing-3,ARRDC3)在肠道病毒D组68型(enterovirus D species,EV-D68)感染A549中的表达以及对A549细胞株生物学行为的影响。方法对EV-D68感染宿主细胞前后的样本进行全转录组高...目的探索含a-Arrestin结构域蛋白3(a-Arrestin-domain-containing-3,ARRDC3)在肠道病毒D组68型(enterovirus D species,EV-D68)感染A549中的表达以及对A549细胞株生物学行为的影响。方法对EV-D68感染宿主细胞前后的样本进行全转录组高通量测序分析,通过生物信息学分析筛选出差异表达基因ARRDC3;RT-qPCR和Western blot验证ARRDC3的表达水平;设计实验分组4组,对照组(未感染EV-D68的A549细胞)、感染组(感染EV-D68的A549细胞)、敲低ARRDC3感染组(感染EV-D68的A549细胞转染ARRDC3-SiRNA-干扰片段)、敲低对照感染组(感染EV-D68的A549细胞转染NC-SiRNA-干扰片段),通过流式细胞术、CCK-8、Transwell实验检测ARRDC3在EV-D68感染模型中对A549细胞周期、增殖、迁移的影响。结果从测序结果中共筛选出差异表达2倍以上的差异表达基因(differentially expressed genes,DEGs)239个,其中上调基因135个,下调基因104个,ARRDC3是差异表达基因之一。EV-D68感染A549后,通过RT-qPCR和Western blot结果发现ARRDC3的表达水平显著增加(P<0.05)。细胞周期明显缩短,抑制细胞迁移。进一步通过转染成功干扰ARRDC3表达载体,沉默ARRDC3可以增强EV-D68感染A549细胞,沉默ARRDC3细胞周期DNA合成期延长(P<0.05),虽然对宿主细胞增殖无显著影响,但沉默ARRDC3可引起细胞迁移能力增强(P<0.05)。结论ARRDC3在EV-D68感染A549后表达明显上调,通过阻滞宿主细胞DNA合成期,抑制宿主细胞迁移等作用来发挥对宿主细胞的影响。展开更多
A retrospective surveillance study on enterovirus D68 was performed in Beijing, China, following the largest and most widespread EV-D68 infection, which occurred in the USA. From January 2011 to July 2015, EV-D68 was ...A retrospective surveillance study on enterovirus D68 was performed in Beijing, China, following the largest and most widespread EV-D68 infection, which occurred in the USA. From January 2011 to July 2015, EV-D68 was identified in 12 individuals with respiratory infections in Beijing, China. The phylogenetic relationships based on the genomic sequence alignment showed that there were two lineages circulating in Beijing from 2011 to 2015. Eight EV-D68 strains belonged to group 1 and four belonged to group 3. All EV-D68 strains from Beijing in 2014 were separately clustered into subgroup II of group 1. Based on these results, we concluded that the Beijing EV-D68 strains had little association with the EV-D68 strains circulating in the 2014 USA outbreak.展开更多
BACKGROUND Acute flaccid paralysis(AFP)and neurogenic respiratory failure rarely occur in children.At the end of 2018,some children with such symptoms were admitted to our hospital.In this study,we aimed to assess two...BACKGROUND Acute flaccid paralysis(AFP)and neurogenic respiratory failure rarely occur in children.At the end of 2018,some children with such symptoms were admitted to our hospital.In this study,we aimed to assess two children with AFP and neurogenic respiratory failure associated with enterovirus D68(EV-D68).CASE SUMMARY Two children admitted to our hospital presented with symptoms and imaging results different from those of acute disseminated encephalomyelitis and hand,foot,and mouth disease.Their main symptoms were AFP and neurogenic respiratory failure.Magnetic resonance imaging showed severe inflammatory injury mainly to the anterior horn cells of the spinal cord.Blood and cerebrospinal fluid samples were collected to assess for pathogens,including bacteria,tuberculosis,cryptococcus,herpes virus,and coxsackie virus,and the results were negative.At the beginning,the two cases were not assessed for EV-D68 in the nasopharyngeal,blood,and cerebrospinal fluid specimens.About 2 mo later,EVD68 was detected in the stool sample of one of the cases.The symptom of AFP was caused by injury to the anterior horn cells at levels C5-L5 of the spinal cord,while neurogenic respiratory failure was at levels C3-C5.CONCLUSION We should pay attention to the detection and diagnosis of EV-D68 and make efforts to develop antivirus drugs and vaccines.展开更多
基金supported by the Beijing Municipal Science and Technology Commission(Z151100003915140)Capital Medical Development and scientific research fund(2016-2-3011)National Major Science and Technology Project for Control and Prevention of Major Infectious Diseases of China(2016ZX10004206)
文摘A retrospective surveillance study on enterovirus D68 was performed in Beijing, China, following the largest and most widespread EV-D68 infection, which occurred in the USA. From January 2011 to July 2015, EV-D68 was identified in 12 individuals with respiratory infections in Beijing, China. The phylogenetic relationships based on the genomic sequence alignment showed that there were two lineages circulating in Beijing from 2011 to 2015. Eight EV-D68 strains belonged to group 1 and four belonged to group 3. All EV-D68 strains from Beijing in 2014 were separately clustered into subgroup II of group 1. Based on these results, we concluded that the Beijing EV-D68 strains had little association with the EV-D68 strains circulating in the 2014 USA outbreak.
文摘BACKGROUND Acute flaccid paralysis(AFP)and neurogenic respiratory failure rarely occur in children.At the end of 2018,some children with such symptoms were admitted to our hospital.In this study,we aimed to assess two children with AFP and neurogenic respiratory failure associated with enterovirus D68(EV-D68).CASE SUMMARY Two children admitted to our hospital presented with symptoms and imaging results different from those of acute disseminated encephalomyelitis and hand,foot,and mouth disease.Their main symptoms were AFP and neurogenic respiratory failure.Magnetic resonance imaging showed severe inflammatory injury mainly to the anterior horn cells of the spinal cord.Blood and cerebrospinal fluid samples were collected to assess for pathogens,including bacteria,tuberculosis,cryptococcus,herpes virus,and coxsackie virus,and the results were negative.At the beginning,the two cases were not assessed for EV-D68 in the nasopharyngeal,blood,and cerebrospinal fluid specimens.About 2 mo later,EVD68 was detected in the stool sample of one of the cases.The symptom of AFP was caused by injury to the anterior horn cells at levels C5-L5 of the spinal cord,while neurogenic respiratory failure was at levels C3-C5.CONCLUSION We should pay attention to the detection and diagnosis of EV-D68 and make efforts to develop antivirus drugs and vaccines.
