副黏病毒V蛋白是由其P基因编码的一种非结构蛋白,能够阻断IFN信号通路,拮抗IFN的抗病毒效应,通常认为是病毒毒力因子之一。在副黏病毒感染过程中,V蛋白靶向性地与IFN信号通路JAK-STAT途径中关键信号转导与转录活化因子(signal transduce...副黏病毒V蛋白是由其P基因编码的一种非结构蛋白,能够阻断IFN信号通路,拮抗IFN的抗病毒效应,通常认为是病毒毒力因子之一。在副黏病毒感染过程中,V蛋白靶向性地与IFN信号通路JAK-STAT途径中关键信号转导与转录活化因子(signal transducer and activator of transcription,STAT)蛋白相互作用,从而发挥拮抗IFN下游信号的功能。不同副黏病毒V蛋白与STAT作用机制也不尽相同。本文对副黏病毒V蛋白产生,IFN信号通路及不同副黏病毒拮抗IFN信号分子机制做一概述。展开更多
本文报告了干扰素诱导跨膜蛋白5(interferon-induced transmembrane protein 5,IFITM5)基因杂合变异导致的Ⅴ型先天性成骨不全(osteogenesis imperfecta,OI)的1家系3例患儿。该三胞胎患儿分别在生后21、16和17 d以气促和多发骨折起病,...本文报告了干扰素诱导跨膜蛋白5(interferon-induced transmembrane protein 5,IFITM5)基因杂合变异导致的Ⅴ型先天性成骨不全(osteogenesis imperfecta,OI)的1家系3例患儿。该三胞胎患儿分别在生后21、16和17 d以气促和多发骨折起病,入院体格检查时均见散在花斑纹、硬肿,三胞胎之二右手腕见数粒疱疹;三胞胎之小口腔可见散在疱疹、溃烂;合并新生儿败血症、休克、呼吸衰竭、新生儿坏死性小肠结肠炎及颅内感染。全外显子测序检测到三胞胎患儿致病变异位于干扰素诱导跨膜蛋白5(interferon-induced transmembrane protein 5,IFITM5)编码基因的5'-非翻译区,1个碱基C转换成T(c.-14C>T)。IFITM5基因相关疾病为Ⅴ型OI,为常染色体显性遗传。结合IFITM5基因变异所致临床表型,3例患儿确诊为Ⅴ型OI。经过呼吸支持、抗感染及对症支持治疗后三胞胎均顺利出院。出院后随访至3岁,三胞胎营养状况良好,大运动发育稍迟缓,均再发不同程度、不同部位的骨折。展开更多
Severe acute respiratory syndrome coronavirus(SARS-Co V) encodes eight accessory proteins, the functions of which are not yet fully understood. SARS-Co V protein 6(P6) is one of the previously studied accessory protei...Severe acute respiratory syndrome coronavirus(SARS-Co V) encodes eight accessory proteins, the functions of which are not yet fully understood. SARS-Co V protein 6(P6) is one of the previously studied accessory proteins that have been documented to enhance viral replication and suppress host interferon(IFN) signaling pathways. Through yeast two-hybrid screening, we identified eight potential cellular P6-interacting proteins from a human spleen c DNA library. For further investigation, we targeted the IFN signaling pathway-mediating protein, N-Myc(and STAT) interactor(Nmi). Its interaction with P6 was confirmed within cells. The results showed that P6 can promote the ubiquitin-dependent proteosomal degradation of Nmi. This study revealed a new mechanism of SARS-Co V P6 in limiting the IFN signaling to promote SARS-Co V survival in host cells.展开更多
文摘副黏病毒V蛋白是由其P基因编码的一种非结构蛋白,能够阻断IFN信号通路,拮抗IFN的抗病毒效应,通常认为是病毒毒力因子之一。在副黏病毒感染过程中,V蛋白靶向性地与IFN信号通路JAK-STAT途径中关键信号转导与转录活化因子(signal transducer and activator of transcription,STAT)蛋白相互作用,从而发挥拮抗IFN下游信号的功能。不同副黏病毒V蛋白与STAT作用机制也不尽相同。本文对副黏病毒V蛋白产生,IFN信号通路及不同副黏病毒拮抗IFN信号分子机制做一概述。
文摘本文报告了干扰素诱导跨膜蛋白5(interferon-induced transmembrane protein 5,IFITM5)基因杂合变异导致的Ⅴ型先天性成骨不全(osteogenesis imperfecta,OI)的1家系3例患儿。该三胞胎患儿分别在生后21、16和17 d以气促和多发骨折起病,入院体格检查时均见散在花斑纹、硬肿,三胞胎之二右手腕见数粒疱疹;三胞胎之小口腔可见散在疱疹、溃烂;合并新生儿败血症、休克、呼吸衰竭、新生儿坏死性小肠结肠炎及颅内感染。全外显子测序检测到三胞胎患儿致病变异位于干扰素诱导跨膜蛋白5(interferon-induced transmembrane protein 5,IFITM5)编码基因的5'-非翻译区,1个碱基C转换成T(c.-14C>T)。IFITM5基因相关疾病为Ⅴ型OI,为常染色体显性遗传。结合IFITM5基因变异所致临床表型,3例患儿确诊为Ⅴ型OI。经过呼吸支持、抗感染及对症支持治疗后三胞胎均顺利出院。出院后随访至3岁,三胞胎营养状况良好,大运动发育稍迟缓,均再发不同程度、不同部位的骨折。
基金supported by China NSFC grants (#31170152 and 81130083)
文摘Severe acute respiratory syndrome coronavirus(SARS-Co V) encodes eight accessory proteins, the functions of which are not yet fully understood. SARS-Co V protein 6(P6) is one of the previously studied accessory proteins that have been documented to enhance viral replication and suppress host interferon(IFN) signaling pathways. Through yeast two-hybrid screening, we identified eight potential cellular P6-interacting proteins from a human spleen c DNA library. For further investigation, we targeted the IFN signaling pathway-mediating protein, N-Myc(and STAT) interactor(Nmi). Its interaction with P6 was confirmed within cells. The results showed that P6 can promote the ubiquitin-dependent proteosomal degradation of Nmi. This study revealed a new mechanism of SARS-Co V P6 in limiting the IFN signaling to promote SARS-Co V survival in host cells.
