ArticleCommunications biology2025
The hepatocyte traffic network in the human hepatitis A virus biological cycle from an evolutionary perspective.
Article in Communications biology, 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
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis A virus (HAV) egresses from hepatocytes cloaked in exosomes (eHAV). However, the traffic network used for its release from polarized hepatocytes is not completely understood. We propose that eHAV biogenesis may follow not only an ESCRT-mediated pathway but also the syndecan-syntenin-ALIX pathway. The Bro1 and the V domains of ALIX bind to the pX extension of VP1 and the VP2-late domains of the unmature capsid, respectively. A Serine-to-Glycine replacement at position 134 of VP2, closely located with the first late domain, facilitates the interaction with ALIX promoting the syndecan-syntenin-ALIX pathway and improving the basolateral egress, preferentially using RAB35. This replacement is conserved in hepatoviruses infecting a wide range of mammalian species, but not in hepatoviruses infecting chimpanzees and humans. An inefficient basolateral egress could be a strategy to escape the antiviral cellular response in apes.
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.