Enterovirus 71 (EV71) infection is one of epidemic disease in children commonly in Taiwan. The clinical manifestation of EV71 infection may include acute respiratory disease, hand foot and mouth disease, herpangina, myocarditis, aseptic meningitis, acute flaccid paralysis, brainstem or cerebellar encephalitis. EV71 infection usually occurs through the fecal¡Voral route, leading to viremia and invasion of the skin and mucosa. Infection is initiated by attachment to putative receptor, which induces conformational changes in the virus that facilitate translocation of the viral RNA into the cytoplasm. Some cell surface molecules have been primarily identified for enterovirus which like poliovirus receptor (CD155), coxsackievirus and adenovirus receptor, Decay accelerating factor (CD55) belong Echoviruses but no EV71 receptor has yet been found. Rhabdomyosarcoma cells were used as a model for EV71 infection. We use two-dimensional gel electrophoresis to analyse membrane fraction from rhabdomyosarcoma cells infected with EV71 at 6 h post infection. Twenty-eight differentially expressed protein spots were identified. Some lipid-associated protein slightly change after EV71 infection that may indicate EV71 infection will change membrane structure of rhabdomyosarcoma cells. And some O-linked glycosylation proteins were also upregulated after EV71 infection. It is interesting to reveal the role of these proteins in early EV71 infection and cell response.