ArticleNPJ vaccines2026
Reduced dengue virus pre-membrane protein-HMGB1 interaction activates host cell transcription to attenuate infection.
Article in NPJ vaccines, 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
14 authors.
Funding
Abstract
To successfully complete an infection lifecycle, viruses have to avoid activating host antiviral and transcriptional responses to avoid disrupting cellular processes and cause premature host cell death. How the host transcriptional response to dengue virus (DENV) infection and its impact on pathogenesis, however, remain unclear. Herein, we examined a pair of DENV-2, where the wild-type strain (16681) elicited few host transcriptional responses following infection, in contrast to its clinically tested attenuated derivative (PDK53 strain). Site-directed mutagenesis studies revealed a single D29V substitution on the pre-membrane (prM) protein, present not in 16681 but in PDK53, that altered transcriptional response to infection. Mechanistically, prM D29V substitution impaired interaction of prM protein with host high mobility group box 1 (HMGB1) protein; wild-type prM-HMGB1 interaction prevented HMGB1 cytoplasmic-nuclear translocation to support transcriptional response to infection. Remarkably, HMGB1 knockdown not only reduced transcriptional response but also slowed virus replication rate, suggesting that HMGB1 also controlled the expression of host factors necessary for DENV replication. Indeed, introducing 29 V to prM increased virus replication rate and transcription of antiviral response genes in both wild-type DENV-3 as well as chimeric DENV-3/-2, the DENV-3 component of TAK-003. Our findings suggest exploiting this interaction to improve immunogenicity and potentially efficacy of current vaccines.
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.