Abstract
BackgroundJapanese encephalitis virus (JEV) is a mosquito-borne flavivirus that causes acute viral encephalitis in humans. Pigs are important amplifiers of JEV. The entry mechanism of JEV into porcine cells remains largely unknown. In this study, we present a study of the internalization mechanism of JEV in porcine kidney epithelial PK15 cells.ResultsWe demonstrated that the disruption of the lipid raft by cholesterol depletion with methyl-β-cyclodextrin (MβCD) reduced JEV infection. We also found that the knockdown of clathrin by small interfering RNA (siRNA) significantly reduced JEV-infected cells and JEV E-glycoprotein levels, suggesting that JEV utilizes clathrin-dependent endocytosis. In contrast, the knockdown of caveolin-1, a principal component of caveolae, had only a small (although statistically significant) effect on JEV infection, however, JEV entry was not affected by genistein. These results suggested that JEV entry was independent of caveolae.ConclusionsTaken together, our results demonstrate that JEV enters porcine kidney epithelial PK15 cells through cholesterol- and clathrin-mediated endocytosis.
Highlights
Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus that causes acute viral encephalitis in humans
We used RNA interference (RNAi) to examine the roles of clathrin and caveolin-1 in the JEV entry process; the results indicated that knockdown of clathrin reduced JEV infection, knockdown of caveolin-1 showed only a small effect on JEV infection and JEV entry was not affected by genistein
JEV infection is inhibited by the depletion of cholesterol Many viruses commonly use lipid rafts to enter host cells
Summary
Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus that causes acute viral encephalitis in humans. Japanese encephalitis virus (JEV) is a mosquito-borne flavivirus that belongs to the family Flaviviridae. JEV is one of the most important endemic encephalitides and can cause acute viral encephalitis, of which there are approximately 50,000 cases in humans annually [1]. The viral RNA encodes a single large polyprotein that is cleaved into three structural proteins, Viruses enter cells through binding cellular receptors. Clathrin-mediated endocytosis (CME) is the best characterized of the endocytic mechanisms, and most viruses utilize this type of endocytosis to enter cells. Recent studies have shown that JEV infects neuronal cells through a clathrin-independent, dynamin- and caveolae-mediated endocytosis pathway [10,11]. Previous studies have found that JEV enters Vero and Huh
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