Key result
Se@PEI@siRNA effectively inhibited EV71 proliferation in SK-N-SH cells, increasing cell viability to 68% compared to 39% in untreated infected cells and reducing apoptosis.
Why the study?
Specific drugs for EV71 are currently lacking, and while siRNA provides a promising antiviral pathway, it struggles to cross cell membranes and degrades easily.
Does Se@PEI@siRNA prevent EV71 infection in SK-N-SH cells?
Does Se@PEI@siRNA prevent EV71 infection in SK-N-SH cells?
Absolute Event Rate: 68% vs 39%
Se@PEI@siRNA demonstrates promising antiviral activity against Enterovirus 71 in vitro by preventing infection and restraining Bax apoptosis signaling.
Enterovirus 71 (EV71) is the principal pathogen leading to severe cases of hand, foot, and mouth disease (HFMD). Specific drugs for EV71 are not discovered currently. Small interfering RNA (siRNA) provides a promising antiviral treatment pathway, but it is difficult to cross cell membranes and is easy to degrade. Nanoparticles are promising for their carrying capacity currently. In this study, the siRNA targeting EV71 VP1 gene was loaded with selenium nanoparticles (SeNPs) and surface decorated with polyethylenimine (PEI) (Se@PEI@siRNA). Se@PEI@siRNA showed a remarkable interference efficiency in the nerve cell line SK-N-SH and prevented the cells to be infected. The mechanism study revealed that Se@PEI@siRNA could lighten the extent of SK-N-SH cells for staying in the sub-G1 phase. Activation of Bax apoptosis signaling was restrained either. Taken together, this study demonstrated that Se@PEI@siRNA is a promising drug against EV71 virus.
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Lin et al. (2020) studied Enterovirus 71 (EV71) infection. Se@PEI@siRNA (selenium nanoparticles loaded with siRNA targeting EV71 VP1 gene) vs. Untreated EV71-infected cells was evaluated on Cell viability after EV71 infection. Se@PEI@siRNA effectively inhibited EV71 proliferation in SK-N-SH cells, increasing cell viability to 68% compared to 39% in untreated infected cells and reducing apoptosis.
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