ReviewBiomolecules2025
Beyond Processing: Furin as a Central Hub in Viral Pathogenesis and Genetic Susceptibility.
Review in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Molecular Aspects of Viral Pathogenesis in Emerging SARS-CoV-2 Variants: Evolving Mechanisms of Infection and Host Response.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Furin, a calcium-dependent serine endoprotease of the proprotein convertase family, plays a pivotal role in both physiological homeostasis and viral pathogenesis. By cleaving polybasic motifs within viral glycoproteins, furin enables the maturation of structural proteins essential for viral entry, fusion, and replication. This mechanism has been documented across a broad spectrum of human pathogens, including SARS-CoV-2, influenza virus, human immunodeficiency virus, human papilloma virus, hepatitis B virus, flaviviruses, herpesviruses, and paramyxoviruses, highlighting furin as a conserved molecular hub in host-virus interactions. Genetic variability within the FURIN gene further modulates infection outcomes. Several single-nucleotide polymorphisms (SNPs), such as rs6226 and rs1981458, are associated with altered COVID-19 severity, whereas variants like rs17514846 confer protection against human papilloma virus infection. Conversely, mutations predicted to reduce enzymatic activity have been linked to attenuated SARS-CoV-2 pathogenesis in certain populations. These findings underscore the importance of considering population genetics when evaluating viral susceptibility and disease progression. Despite advances, unresolved questions remain regarding furin's non-canonical roles in viral life cycles, tissue-specific regulation, and interactions with other host proteases and immune modulators. Targeted inhibition of furin and related convertases represents a promising avenue for broad-spectrum antiviral interventions. Collectively, current evidence positions furin as a central node at the intersection of viral pathogenesis, host genetic variability, and translational therapeutic potential.
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What Socratic 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 Socratic graph.