ArticleBMC infectious diseases2026
Circular RNA SETD2 (circSETD2) elevates DDX3 expression to inhibit autophagy in hepatitis B virus infection via targeting miR-181a-5p.
Article in BMC infectious diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatitis B virus (HBV) is one of the major causes for chronic liver disease leading to cirrhosis and hepatocellular carcinoma (HCC). It utilizes the host cell machinery, such as host factors and non-coding RNAs, to modulate its survival and proliferation. CircRNAs, a special class of non-coding RNAs, play a crucial role in regulating HBV infection. A recent study reported that circular RNA SET domain containing 2 (circSETD2) was down-regulated in HCC, however, there is no study available on its role in modulating HBV-infection.
methodsThe hepatic cell lines were cultured in DMEM with 10% FBS and antibiotics. HepG2 cells were transfected with empty vector, HBV or HBx expression plasmids. HepG2.2.15 cells were transfected with non-specific RNA, circSETD2, miR-181a-5p mimic or miR-181a-5p inhibitor. The expression of circSETD2 and miR-181a-5p were determined by qPCR, and Western blots were performed for analyzing autophagic marker proteins. Autophagy flux assays were performed in circSETD2, miR-181a-5p mimic or miR-181a-5p inhibitor-transfected cells. Significance of the data were analyzed using unpaired student t-test.
resultsThe expression of circSETD2 was significantly lower (76%) in HepG2.215 cells, compared to non-HBV infected cells. Overexpression of HBV and HBx in HepG2 cells significantly reduced the expression of circSETD2. CircSETD2 overexpression decreased the HBsAg levels and the expression of miR-181a-5p. Overexpression of miR-181a-5p decreased Dead-Box RNA Helicase 3 (DDX3) expression and induced autophagy proteins. Inhibition of miR-181a-5p enhanced the expression of DDX3, which led to decreased autophagy. Overexpression of circSETD2 increased the expression of DDX3 and decreased autophagy proteins.
conclusionThe data showed that HBx suppressed circSETD2 to induce miR-181a-5p expression, which in turn resulted in the decreased DDX3, leading to the increased autophagy in HBV-infected hepatic cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.