What question did this study set out to answer?

To investigate the role of USP17L13 in influenza A virus replication and its interactions with the innate immune system.

May 22, 2026VirusesOpen Access

USP17L13 Enhances Influenza a Virus Replication by Mediating the Degradation of RIG-I and MDA5

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Authors

YZY ZHANGSouth China Agricultural University CQChen QinChinese Academy of Agricultural Sciences YZYichao ZhuangChinese Academy of Agricultural Engineering

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Implication

Genome-wide screen identifies USP17L13 as a negative regulator of innate immunity, enhancing influenza virus replication in human lung cells, suggesting new therapeutic targets.

Key Points

To investigate the role of USP17L13 in influenza A virus replication and its interactions with the innate immune system.
Performed a genome-wide CRISPR/dCas9 gene activation screen in human lung epithelial A549 cells.
Analyzed the effect of USP17L13 on viral replication and host antiviral defenses using transcriptomic analysis.
Examined the degradation of RIG-I and MDA5 in response to USP17L13 overexpression.
Overexpression of USP17L13 increased replication of multiple influenza virus subtypes in A549 cells.
USP17L13 promotes degradation of RIG-I and MDA5, leading to impaired host interferon responses.
Transcriptomic analysis showed downregulation of NF-kB signaling and upregulation of pathways facilitating viral production.

Cite This Study

ZHANG et al. (2026) studied this question.

synapsesocial.com/papers/6a0ff351d674f7c03778be4c https://doi.org/10.3390/v18050575

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Implication

Genome-wide screen identifies USP17L13 as a negative regulator of innate immunity, enhancing influenza virus replication in human lung cells, suggesting new therapeutic targets.

USP17L13 Enhances Influenza a Virus Replication by Mediating the Degradation of RIG-I and MDA5

Discussion

Member takes

Implication

Key Points

Cite This Study

USP17L13 Enhances Influenza a Virus Replication by Mediating the Degradation of RIG-I and MDA5

Discussion

Member takes

Implication

Key Points

Cite This Study

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