December 18, 2021VirulenceOpen Access

Seneca Valley virus 3C pro degrades heterogeneous nuclear ribonucleoprotein A1 to facilitate viral replication

Q: What is the clinical evidence from this study?

Study design: Other. Population: Seneca Valley virus infection. Intervention: Seneca Valley virus infection and 3C protease vs. Mock-infected cells. Primary outcome: hnRNP A1 redistribution and degradation.

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Key result

Seneca Valley virus 3C protease induces the degradation and cytoplasmic translocation of cellular hnRNP A1 via the proteasome pathway to facilitate viral replication.

Why the study?

Whether heterogeneous nuclear ribonucleoprotein A1 is involved in Seneca Valley virus replication was unknown.

Design

In vitro experimental study

Authors

JSJiangwei Song DWDan Wang RQRong Quan

Discussion

Member takes

Overview

May inform SVV antiviral development via 3C protease inhibition; animal data leaves open clinical translation.

Structured PICO

Population

In vitro cell models infected with Seneca Valley virus (SVV)

Intervention

Seneca Valley virus (SVV) infection, siRNA-mediated knockdown of hnRNP A1, overexpression of hnRNP A1, proteasome inhibitor (MG132), and inactivation of the conserved catalytic box in 3Cpro

Comparator

Mock-infected cells and untreated controls

Outcome

Viral replication, hnRNP A1 redistribution, and hnRNP A1 degradationsurrogate

SVV 3C protease targets cellular hnRNP A1 for degradation and translocation to aid viral replication, revealing a potential target for controlling SVV infection.

Cite This Study

Song et al. (2021) studied Seneca Valley virus infection. Seneca Valley virus infection and 3C protease vs. Mock-infected cells was evaluated on hnRNP A1 redistribution and degradation. Seneca Valley virus 3C protease induces the degradation and cytoplasmic translocation of cellular hnRNP A1 via the proteasome pathway to facilitate viral replication.

synapsesocial.com/papers/6a9484138a4c78aef331af50 https://doi.org/10.1080/21505594.2021.2014681

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December 18, 2021VirulenceOpen Access

Seneca Valley virus 3C pro degrades heterogeneous nuclear ribonucleoprotein A1 to facilitate viral replication

View Full Paper

Ask AI

Bookmark

Key result

Seneca Valley virus 3C protease induces the degradation and cytoplasmic translocation of cellular hnRNP A1 via the proteasome pathway to facilitate viral replication.

Why the study?

Whether heterogeneous nuclear ribonucleoprotein A1 is involved in Seneca Valley virus replication was unknown.

Design

In vitro experimental study

Authors

JSJiangwei Song DWDan Wang RQRong Quan

Discussion

Member takes

Overview

May inform SVV antiviral development via 3C protease inhibition; animal data leaves open clinical translation.

Structured PICO

Population

In vitro cell models infected with Seneca Valley virus (SVV)

Intervention

Seneca Valley virus (SVV) infection, siRNA-mediated knockdown of hnRNP A1, overexpression of hnRNP A1, proteasome inhibitor (MG132), and inactivation of the conserved catalytic box in 3Cpro

Comparator

Mock-infected cells and untreated controls

Outcome

Viral replication, hnRNP A1 redistribution, and hnRNP A1 degradationsurrogate

SVV 3C protease targets cellular hnRNP A1 for degradation and translocation to aid viral replication, revealing a potential target for controlling SVV infection.

Cite This Study

synapsesocial.com/papers/6a9484138a4c78aef331af50 https://doi.org/10.1080/21505594.2021.2014681

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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