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Peru reports the highest global ATLL incidence, yet comprehensive genomic studies remain limited. We aimed to characterize the virological, immunological, and host genetic landscape of HTLV-1 infection to identify population-specific high-risk features.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We conducted a prospective cohort study (2017\u20132018) of 67 HTLV-1-infected individuals from Lima, Peru, using an integrated high-throughput genomic approach. This included whole-genome HTLV-1 sequencing, targeted ultra-deep sequencing of 280 hematological malignancy-associated genes, high-resolution HLA typing, GATK-based variant calling, and comprehensive clinical follow-up over 7 years. Phylogenomic analyses were performed using maximum likelihood and Bayesian approaches.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The cohort exhibited exceptionally high-risk characteristics with a median proviral load (PVL) of 4.5\u2009\u00b1\u20093.8, and 13.4% cumulative crude mortality over 7 years. Phylogenomic analysis revealed 96.8% of isolates belonged to the Transcontinental subtype, with most clustering in a newly identified Andean-Amazonian subgroup. HLA-I analysis demonstrated unique population-specific allele distributions with significantly reduced evolutionary divergence compared to Japanese cohorts (HLA-HED: 5.34 vs. 6.87,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.0002), potentially differences in mechanisms of viral immune control. Ultra-deep sequencing identified early clonal hematopoiesis with prevalent mutations in cancer-associated genes including KMT2D (55%), NOTCH1 (49%), and TP53 (27%). Mutation burden correlated significantly with proviral load (\n                      <jats:italic>r<\/jats:italic>\n                      \u2009=\u20090.34,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.003), and longitudinal analysis revealed progressive genomic instability with more than two-fold increase in mutations over 3 years (7.25 vs. 19.5 mutations per patient,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.01). High PVL (&gt;\u20094%) was the only independent predictor of crude mortality (OR: 1.07; 95% CI: 1.01\u20131.15;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.033). Contrary to previous reports,\n                      <jats:italic>Strongyloides<\/jats:italic>\n                      coinfection was not associated with disease progression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>This first comprehensive genomic characterization of HTLV-1 in South America reveals population-specific viral evolution, reduced HLA diversity, and evidence of early oncogenic transformation events. The exceptionally high proviral loads and unique mutational landscape provide novel insights into HTLV-1 pathogenesis and support the development of population-tailored risk stratification approaches. These findings emphasize the urgent need for expanded genomic surveillance and targeted interventions in underrepresented populations bearing disproportionate HTLV-1 burden.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12985-026-03148-8","type":"journal-article","created":{"date-parts":[[2026,4,6]],"date-time":"2026-04-06T15:55:21Z","timestamp":1775490921000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The viral and host genomic landscape of human T-cell leukemia virus type I in Peru"],"prefix":"10.1186","volume":"23","author":[{"given":"Daniel","family":"Enriquez-Vera","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jiazhou","family":"Li","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jorge","family":"Nakazaki-Aza","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kosuke","family":"Mochida","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yutaka","family":"Suzuki","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eduardo","family":"Gotuzzo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mart\u00edn","family":"Montes","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kazuhiro","family":"Morishita","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shingo","family":"Nakahata","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2026,4,6]]},"reference":[{"key":"3148_CR1","doi-asserted-by":"crossref","unstructured":"Bangham CRM. 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