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Abstract
The productive infection of influenza A virus (IAV) depends on host factors. However, the involvement of long non-coding RNAs (lncRNAs) in IAV infection remains largely uninvestigated. In this work, we have discovered a human lncRNA, named lncRNA-PAAN (PA-associated noncoding RNA) that enhances IAV replication. The level of lncRNA-PAAN increases upon infection of IAV, but not other viruses, nor interferon treatment, suggesting specific up-regulation of lncRNA-PAAN expression by IAV. Silencing lncRNA-PAAN significantly decreases IAV replication through impairing the activity of viral RNA-dependent RNA polymerase (RdRp). This function of lncRNA-PAAN is a result of its association with viral PA protein, a key component of IAV RNA polymerase complex. Consequently, depletion of lncRNA-PAAN prevents the formation of functional RdRp. Together, these results suggest that lncRNA-PAAN promotes the assembly of viral RNA polymerase, thus warranting efficient viral RNA synthesis. Elucidating the functions of lncRNAs in IAV infection is expected to advance our understanding of IAV pathogenesis and open new avenues to the development of novel anti-IAV therapeutics.
Highlights
Influenza A virus (IAV) infection causes serious respiratory disease and mortality
The screen was conducted in 293T-Gluc cells that express Gaussia luciferase (Gluc) upon influenza A virus (IAV) infection
The cells were first transfected with esiRNAs prior to infection with IAV, followed by measuring the Gluc activity that reflecting the level of IAV infection
Summary
Influenza A virus (IAV) infection causes serious respiratory disease and mortality. IAV belongs to Orthomyxoviridae, contains eight segments of single-stranded negative-sense RNA (vRNA) that together encode more than 10 viral proteins including several splice variants. Each vRNA is coated with viral nucleoprotein (NP), its 50 and 30 ends are bound by a single copy of viral RNA-dependent RNA polymerase (RdRp) complex. RNA transcription (vRNA to mRNA) and replication (vRNA to cRNA to vRNA) [4,5,6]. IAV infection begins with the viral hemagglutinin (HA) protein binding to the sailic acid at the surface of host cell, followed virion internalization and fusion of cellular and viral membranes. Viral ribonucleoprotein (vRNP) is released into the cytosol, and further imported into the nucleus where transcription
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