ArticlePLoS pathogens2024
A small protein encoded by PCBP1-AS1 is identified as a key regulator of influenza virus replication via enhancing autophagy.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- In vitro and in vivo studies of GAPLINC identify it as a critical host factor involved in the regulation of influenza A virus infection.Veterinary research · 2026Article
- Bamboo polyphenols protects against Escherichia coli-induced liver injury in broilers by attenuating inflammatory responses.Poultry science · 2026Article
- IRES-like element-mediated translation of vsp1S4(-) suppresses BmCPV replication via RNAi antagonism.PLoS pathogens · 2026Article
- The Janus face of host LncRNA in viral infections: Defender or collaborator?Communications biology · 2026Review
- Sorting Nexin 10 Mediates Endosomal Acidification and Autophagy to Promote Influenza A Virus Infection.Viruses · 2026Article
- Article
- Microproteins in Human Physiology and Pathology.Biochemistry · 2026Review
- Cysteine Reactivity Profiling Identifies Host Regulators ofACS infectious diseases · 2026Article
- Long Non-Coding RNAs Can Govern the Antiviral Immune Response Through Interferon-Mediated Mechanisms in Respiratory Tract.Viruses · 2026Review
- The dynamic interplay between viruses and host non-coding RNA species.FEMS microbiology reviews · 2026Review
- Non-coding RNAs: master regulators in the battle between host antiviral defense and viral replication.Frontiers in immunology · 2026Review
- The lncRNA GAS5-encoded micropeptide facilitates influenza virus replication through modulation of the Wnt/β-catenin signaling pathway.Current research in microbial sciences · 2026Article
- A chicken lncRNA is identified as a critical regulator that increases influenza virus replication by impairing innate antiviral responses.Veterinary research · 2025Article
- Cysteine reactivity profiling identifies host regulators ofbioRxiv : the preprint server for biology · 2025Article
- THAP11-mediated K48- and K63-linked ubiquitination is essential for the degradation of porcine reproductive and respiratory syndrome virus nonstructural protein 1β.Cellular and molecular life sciences : CMLS · 2025Article
- Current Perspectives on Functional Involvement of Micropeptides in Virus-Host Interactions.International journal of molecular sciences · 2025Review
- Autophagy and Respiratory Viruses: Mechanisms, Viral Exploitation, and Therapeutic Insights.Cells · 2025Review
- Long Non-Coding RNA THRIL Promotes Influenza Virus Replication by Inhibiting the Antiviral Innate Immune Response.Viruses · 2025Article
- The regulatory roles of STAT3 protein in the pathogenesis of viral infections.Frontiers in cellular and infection microbiology · 2025Review
- The role of long non-coding RNAs and circular RNAs in immune evasion of influenza A virus: recent advances.Frontiers in cellular and infection microbiology · 2025Review
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10 authors.
Funding
Abstract
Many annotated long noncoding RNAs (lncRNAs) contain small open reading frames (sORFs), some of which have been demonstrated to encode small proteins or micropeptides with fundamental biological importance. However, functions of lncRNAs-encoded small proteins or micropeptides in viral pathogenesis remain largely unexplored. Here, we identified a 110-amino acid small protein as a key regulator of influenza A virus (IAV) replication. This small protein that we call PESP was encoded by the putative lncRNA PCBP1-AS1. It was observed that both PCBP1-AS1 and PESP were significantly upregulated by IAV infection. Furthermore, they were markedly induced by treatment with either type I or type III interferon. Overexpression of either PCBP1-AS1 or PESP alone significantly enhanced IAV replication. In contrast, shRNA-mediated knockdown of PCBP1-AS1 or CRISPR/Cas9-mediated knockout of PESP markedly inhibited the viral production. Moreover, the targeted deletion or mutation of the sORF within the PCBP1-AS1 transcript, which resulted in the disruption of PESP expression, significantly diminished the capacity of PCBP1-AS1 to enhance IAV replication, underscoring the indispensable role of PESP in the facilitation of IAV replication by PCBP1-AS1. Interestingly, overexpression of PESP enhanced the IAV-induced autophagy by increasing the expression of ATG7, an essential autophagy effector enzyme. We also found that the 7-22 amino acids at the N-terminus of PESP were crucial for its functionality in modulating ATG7 expression and action as an enhancer of IAV replication. Additionally, HSP90AA1, a protein identified previously as a facilitator of autophagy, was found to interact with PESP, resulting in the stabilization of PESP and consequently an increase in the production of IAV. These data reveal a critical lncRNA-encoded small protein that is induced and exploited by IAV during its infection, and provide a significant insight into IAV-host interaction network.
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