Objective: 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.
Methods: 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.
Results: EV71 infection enhances the type conversion of LC3 and degradation of P62. The infectious virus particles were decreased after the treatment of 3-MA.
Conclusion: EV71 infection could induce cell autophagy and the autophagy might contribute to the production and release of infectious EV71 particles.
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