肠道病毒71型(enterovirus 71, EV71)感染常导致婴幼儿手足口病(hand, foot and mouth disease, HFMD)，细菌脂多糖(lipopolysaccharide, LPS)在多种肠道病毒感染过程中起重要作用。本研究旨在探讨细菌LPS对EV71感染的影响。将EV71与LPS共孵育，测定病毒被热处理后残留病毒的活力，以及病毒感染过程中病毒基因拷贝数的变化。结果显示，热处理后病毒活力逐渐丧失，而经LPS处理的病毒活力丧失的速度减缓，且残留病毒活力与LPS浓度呈正相关；LPS处理后的病毒在黏附、侵入、胞内复制及释放过程中基因拷贝数较对照组均降低；免疫印迹分析表明LPS与抗VP1单克隆抗体可竞争性结合EV71，且粪便中的EV71可被抗大肠埃希菌抗体识别。上述结果提示，LPS可增强EV71热稳定性，抑制EV71感染过程，且LPS可能与EV71结合。

Enterovirus 71 (EV71) infection mainly causes hand-foot-mouth disease (HFMD) in infants and young children. There are many commensal bacteria in the environment of viral infection. It was reported that lipopolysaccharide (LPS) plays an important role in some enterovirus infections. This study aims to investigate the effects of LPS on EV71 infection. EV71 was co-incubated with LPS to determine its impact on the viral viability and infectivity. Results showed that LPS-incubated EV71 lost their viability slower than that of the EV71 control in a LPS concentration-dependent manner. In contrast, the infectivity of EV71 decreased when the virus was pretreated by LPS. The immunoblotting assay showed that LPS could bind with EV71 competitively with anti-VP1. EV71 from HFMD patients can be detected by anti-E.coli antibodies. The observations indicated that LPS can increase the thermal stability of EV71 and inhibit viral infection. Both effects might be ascribed to the capability of LPS binding with the virus.