What is the clinical evidence from this study?

Study design: Other. Population: Enterovirus A71 infection. Intervention: Enterovirus A71 infection vs. Mock infection. Primary outcome: Autophagy induction and viral RNA replication.

What does this research mean for the field?

Enterovirus A71 infection induces autophagy and autophagic flux without triggering apoptosis in human neuronal cells, facilitating viral RNA replication through autophagosome production. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

September 17, 2020Scientific ReportsOpen Access

Autophagy is induced and supports virus replication in Enterovirus A71-infected human primary neuronal cells

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Key result

Enterovirus A71 infection induces autophagy without apoptosis in human neuronal cells to support viral replication.

Why the study?

The effect of Enterovirus A71 infection on human neuronal cells remains poorly understood.

Population

Human neural stem cells and IMR-32 neuroblastoma cells differentiated into neuronal cells

Comparison

Enterovirus A71 infection vs no infection

Design

Preclinical laboratory study

Authors

JLJhao‐Yin Lin HHHsing‐I Huang

Discussion

Member takes

Overview

No immediate change to EV-A71 care; leaves open autophagy modulation as a replication target for future study.

Structured PICO

Population

In vitro study using human neural stem cells and IMR-32 neuroblastoma cells differentiated into neuronal cells to investigate the cellular effects of Enterovirus A71 infection.

Intervention

Enterovirus A71 (EV-A71) infection

Outcome

Effect of EV-A71 infection on neuronal cells (cytopathic effect, apoptosis, autophagy, and viral replication)surrogate

EV-A71 infection induces autophagy in human neuronal cells, which supports viral RNA replication without causing obvious cytopathic effects or apoptosis.

Cite This Study

Lin et al. (2020) studied Enterovirus A71 infection. Enterovirus A71 infection vs. Mock infection was evaluated on Autophagy induction and viral RNA replication. Enterovirus A71 infection induces autophagy and autophagic flux without causing apoptosis in human neuronal cells, and the accumulation of autophagosomes supports viral RNA replication.

synapsesocial.com/papers/6ab08ab05bb37f32599593e6 https://doi.org/10.1038/s41598-020-71970-3

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September 17, 2020Scientific ReportsOpen Access

Autophagy is induced and supports virus replication in Enterovirus A71-infected human primary neuronal cells

View Full Paper

Ask AI

Bookmark

Key result

Enterovirus A71 infection induces autophagy without apoptosis in human neuronal cells to support viral replication.

Why the study?

The effect of Enterovirus A71 infection on human neuronal cells remains poorly understood.

Population

Human neural stem cells and IMR-32 neuroblastoma cells differentiated into neuronal cells

Comparison

Enterovirus A71 infection vs no infection

Design

Preclinical laboratory study

Authors

JLJhao‐Yin Lin HHHsing‐I Huang

Discussion

Member takes

Overview

No immediate change to EV-A71 care; leaves open autophagy modulation as a replication target for future study.

Structured PICO

Population

In vitro study using human neural stem cells and IMR-32 neuroblastoma cells differentiated into neuronal cells to investigate the cellular effects of Enterovirus A71 infection.

Intervention

Enterovirus A71 (EV-A71) infection

Outcome

Effect of EV-A71 infection on neuronal cells (cytopathic effect, apoptosis, autophagy, and viral replication)surrogate

EV-A71 infection induces autophagy in human neuronal cells, which supports viral RNA replication without causing obvious cytopathic effects or apoptosis.

Cite This Study

synapsesocial.com/papers/6ab08ab05bb37f32599593e6 https://doi.org/10.1038/s41598-020-71970-3

Also Consider

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