ReviewVirus genes2025
Insights of HIV-1 and HBV transcriptional regulation by viral transactivator Tat and HBx.
Review in Virus genes, 2025. 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
3 authors.
Funding
Abstract
Transcriptions of nascent HIV-1 RNA from the integrated proviral DNA, and HBV RNAs from a stably formed minichromosome of cccDNA, are carried out by cellular RNA polymerase II, and strongly regulated by viral transactivation proteins Tat and HBx, respectively. Both Tat and HBx are intrinsically disordered proteins with promiscuous gene transactivation activities and regulate HIV-1 and HBV transcription by multiple, but similar mechanisms. The antiviral therapies of HIV-1 and HBV effectively suppress viral replication and enable the infection into latent states. The viral life cycles of HIV-1 and HBV differ significantly, but the core mechanisms of T-cell depletion are intertwined. Consequently, future therapeutic interventions must encompass a dual strategy of viral clearance and immune reconstitution. A functional cure would be achieved by combining checkpoint inhibitors, specific T-cell activators, and drugs targeting viral persistence.
Indexed as
Identifiers
40794154What 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.