ArticleVirulence2026
The long noncoding RNA MAPKAPK5-AS1 promotes the formation of hepatitis B virus cccDNA by modulating the expression of NABP1.
Article in Virulence, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular long noncoding RNAs (lncRNAs) have been shown to participate in diverse biological pathways, including the regulation of virus infections. However, their functions in the hepatitis B virus (HBV) life cycle still need to be explored. Here, we conducted a loss-of-function screen targeting 1779 human lncRNAs and identified 19 lncRNAs associated with HBV infection. One lncRNA, named MAPKAPK5-AS1 (lnc-MAAS), was identified as a host factor required for HBV infection. Our data suggest that lnc-MAAS is involved in the conversion of HBV relaxed circular DNA into covalently closed circular DNA (cccDNA). Furthermore, mechanistic experiments revealed that lnc-MAAS affects cccDNA formation by modulating the expression of nucleic acid binding protein 1 (NABP1). Together, our findings shed light on the roles of host lnc-MAAS and NABP1 in HBV cccDNA formation, which may contribute to the development of novel anti-HBV therapeutics.
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