{
  "abstract": "Human antiviral restriction factors act across multiple stages of viral replication, but whether their population-resolved haplotype architecture differs systematically from comparable genomic regions is unclear. We tested this using phased public human genomic data from 660 individuals in seven African and African-diaspora populations, representing 30 canonical restriction-factor units and 436 target windows. Each canonical unit was compared with 80 exact matched genomic controls, yielding 2,400 frozen controls and 4,429,760 target-control endpoint comparisons across 19 retained haplotype endpoints. All 30 canonical units showed lower differentiation effects and lower robust population-private haplotype effects than their matched controls. Within-population diversity effects were higher in 19 of 30 units, whereas dominant-haplotype concentration effects were lower in 22 of 30. Nineteen units occupied a deconcentrated/high-diversity state, eight a concentrated/low-diversity state, and three a lower-diversity/lower-concentration state. Of 127 global endpoint/context summaries, 88 reached a global false-discovery-rate q value below 0.05; 76 were lower in restriction-factor targets and 12 were higher. Directional sign-test inference detected widespread repeated displacement relative to matched controls, whereas no matched-cell empirical-rank test reached global false-discovery-rate significance. These results show that human antiviral restriction-factor loci occupy a reproducible matched-control haplotype architecture characterized by attenuated population partitioning and reduced robust private structure, together with substantial locus-specific variation in within-population diversity and haplotype concentration. The comparative framework separates population-genomic structure from claims of functional or adaptive causality.",
  "abstract_shown": true,
  "affiliations": [
    "St. Francis University College of Health and Allied Sciences (SFUCHAS)"
  ],
  "article_type": "New results",
  "arxiv": null,
  "author_total": 3,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "R. S. Maghembe"
    },
    {
      "name": "S. Y. Bahati"
    },
    {
      "name": "A. Makaranga"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/0h7744q8jyqr2.bib",
  "cited_by": 0,
  "doi": "10.64898/2026.09.01.748667",
  "fulltext_url": "https://www.biorxiv.org/content/10.64898/2026.09.01.748667v1.full",
  "id": "0h7744q8jyqr2",
  "issns": [],
  "landing_url": "https://www.biorxiv.org/content/10.64898/2026.09.01.748667v1",
  "language": null,
  "licence": "CC-BY",
  "licence_label": "CC BY",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "biorxiv",
      "bioinformatics"
    ],
    [
      "openalex",
      "1311|Genetic Associations and Epidemiology"
    ]
  ],
  "openalex": "W7202356624",
  "pdf_url": "https://www.biorxiv.org/content/10.64898/2026.09.01.748667v1.full.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-09-01",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/0h7744q8jyqr2.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:19:33Z",
      "native_id": "10.64898/2026.09.01.748667",
      "source": "biorxiv",
      "url": "https://www.biorxiv.org/content/10.64898/2026.09.01.748667v1"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "biorxiv:bioinformatics",
      "subfield": "bioinformatics"
    }
  ],
  "title": "Restrictome-EVOLVE: population-resolved haplotype architecture of human antiviral restriction-factor loci",
  "title_text": "Restrictome-EVOLVE: population-resolved haplotype architecture of human antiviral restriction-factor loci",
  "type": "preprint",
  "updated_at": "2026-10-30T12:19:33Z",
  "url": "https://research.draconitic.com/paper/0h7744q8jyqr2",
  "venue": "bioRxiv",
  "versions": []
}