ArticleCell reports2025
Interplay of host and viral genetic variations in modulating antibody responses to genotype 3a hepatitis C virus: Implications for vaccine design.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Implications of RNA virus persistence for post-acute sequelae and chronic inflammatory syndromes.Nature immunology · 2026Review
- [Progress in clinical research related to viral hepatitis in 2025].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
Hepatitis C virus (HCV) exhibits significant genetic diversity and is a cause of severe liver complications. The viral envelope glycoproteins E1 and E2, key targets for neutralizing antibodies, are highly variable. To understand how host and viral genetic factors modulate antibody responses, we analyze genetic and antibody binding and neutralization data from 54 patients infected with HCV genotype 3a. We find that host polymorphisms in IFNL4 gene (IFNλ4-P70 generating haplotype) are associated with reduced antibody binding. Within the virus, variations at three specific E1/E2 amino acid positions and three N-glycosylation sites (including one site common to both analyses) significantly correlate with antibody binding and/or neutralization sensitivity. Furthermore, greater intra-patient diversity within the E2 hypervariable region 1 is associated with stronger antibody binding. These results identify specific host and viral genetic features that shape humoral immunity against HCV genotype 3a, providing insights crucial for designing broadly effective vaccines.
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Registered trials
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