Autophagy in coxsackievirus-infected neurons

Seung Yong Yoon, Young Eun Ha, Jung Eun Choi, Jeonghyun Ahn, Heuiran Lee, Dong Hou Kim

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Autophagy is a process to engulf aberrant organelles or protein aggregates into double-membrane vesicles for lysosomal breakdown. Autophagy is a protective process against some intracellular bacteria and viruses; however, it is also used for replication by some viruses, such as poliovirus. We recently found that coxsackievirus B4 (CVB4) also induces the autophagy pathway and activates the calpain system for replication in neurons. Notably, the inhibition of autophagy with 3-methyladenine (3MA) reduced calpain activation and virus replication. Calpain inhibitors also reduced autophago-some formation and virus replication. This finding indicates that calpain and the autophagy pathway are closely connected with each other during the infection. Interestingly, we also found that 3MA and calpain inhibitors enhanced the caspase-3 specific cleavage of spectrin during CVB4 infection, suggesting that autophagy inhibition by these drugs triggered apoptosis. Thus, autophagy and apoptosis may balance each other in CVB4-infected neurons. Here, we show that inhibition of caspase with zVAD increased autopha-gosome formation, further proposing the cross-talk between autophagy and apoptosis in CVB4-infected neurons.

Original languageEnglish (US)
Pages (from-to)388-389
Number of pages2
Issue number3
StatePublished - Apr 1 2009
Externally publishedYes


  • Autophagy
  • Calpain
  • Caspase
  • Coxsackievirus
  • Neuron

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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