Zhang Xiao-Yan, Xi Xue-Yan, Zhao Zhen-Dong
State Key Lab for Molecular Virology and Genetic Engineering, Institute of Pathogen Biology, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing 100005, China.
Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi. 2011 Jun;25(3):176-8.
To determine whether or not enterovirus 71 (enteroviurs 71, EV71) may induce autophagy and affect the production and release of EV71 after the treatment of autophagy inhibitor.
Western blots were performed to examine the conversion of LC3-I to LC3- II and the degradation of P62 after the RD-A cells were infected with EV71. CCID50 was determined by checking the virus titer in the supernatant of cells that treated with autophagy inhibitor 3-MA.
EV71 infection enhances the type conversion of LC3 and degradation of P62. The infectious virus particles were decreased after the treatment of 3-MA.
EV71 infection could induce cell autophagy and the autophagy might contribute to the production and release of infectious EV71 particles.
确定肠道病毒71型（EV71）感染是否可诱导自噬，以及自噬抑制剂处理后对EV71产生和释放的影响。
用EV71感染RD-A细胞后，采用蛋白质免疫印迹法检测微管相关蛋白轻链3（LC3）-Ⅰ向LC3-Ⅱ的转化及P62的降解情况。通过检测自噬抑制剂3-甲基腺嘌呤（3-MA）处理后细胞上清液中的病毒滴度来测定半数细胞感染量（CCID50）。
EV71感染增强了LC3的类型转化和P62的降解。用3-MA处理后，感染性病毒颗粒减少。
EV71感染可诱导细胞自噬，且自噬可能有助于感染性EV71颗粒的产生和释放。
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