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Cell. Infect. Microbiol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>People living with HIV (PLWH) exhibit gut dysbiosis and chronic immune activation. The early dynamics of the gut-immune axis during the transition from diagnosis to viral suppression remain incompletely understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We characterized fecal microbiota (16S rRNA), bacterial translocation (16S rDNA) and gut barrier integrity (serum intestinal fatty acid-binding protein, I-FABP, level) in newly diagnosed PLWH at baseline (t0) and after six months of suppressive ART (t6), compared to uninfected controls. Systemic inflammation (serum concentrations of interleukins 6 and 10, soluble CD163), and peripheral blood T-cell activation were also analyzed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Alpha diversity was similar across groups (p&amp;gt;0.05); beta diversity differed significantly between PLWH at t0 and controls (p=0.002). Linear Discriminant Analysis Effect Size (LEfSe) analysis identified an enrichment of short chain fatty acids (SCFA)-producing genera (\n                      <jats:italic>Alloprevotella<\/jats:italic>\n                      ,\n                      <jats:italic>Mitsuokella<\/jats:italic>\n                      ,\n                      <jats:italic>Succinivibrio<\/jats:italic>\n                      ,\n                      <jats:italic>Megasphaera<\/jats:italic>\n                      ) in PLWH at t0. PLWH at t0 showed elevated bacterial translocation [16S rDNA, 4281 (4018-4485) vs 2162 (2023-2286) copies\/mL, p&amp;lt;0.001], gut barrier damage [I-FABP, 950 (800-1168) vs 767 (574-902) ng\/mL, p=0.012], inflammation [IL-6, 4.8 (3.1-8.8) vs 0.8 (0.3-1.3) pg\/mL, p&amp;lt;0.001; sCD163, 1173 (872-1417) vs 561 (425-662) ng\/mL, p&amp;lt;0.001], and T-cell activation [CD4\n                      <jats:sup>+<\/jats:sup>\n                      CD38\n                      <jats:sup>+<\/jats:sup>\n                      HLA-DR\n                      <jats:sup>+<\/jats:sup>\n                      (percentage of CD4\n                      <jats:sup>+<\/jats:sup>\n                      T lymphocytes), 9.7 (2.8-18.5) vs 1.3 (0.3-2.2), p=0.007; CD8\n                      <jats:sup>+<\/jats:sup>\n                      CD38\n                      <jats:sup>+<\/jats:sup>\n                      HLA-DR\n                      <jats:sup>+<\/jats:sup>\n                      (percentage of CD8+T lymphocytes), 19.0 (12.0-31.1) vs 1.7 (0.6-5.7), p=0.005], compared with controls. Treated PLWH (t6) showed similar alpha and beta diversities of fecal microbiota compared to untreated PLWH (p&amp;gt;0.05 in each case). LEfSe analysis identified an enrichment of\n                      <jats:italic>Campylobacter<\/jats:italic>\n                      and\n                      <jats:italic>Atopobium<\/jats:italic>\n                      at t6. ART mitigates systemic inflammation [t6 vs t0, IL-6, 3.3 (1.7-4.0) vs 4.8 (3.1-8.8) pg\/mL, p=0.022; sCD163, 795 (549-915) vs 1173 (872-1417) ng\/mL, p&amp;lt;0.001], and T-cell activation [t6 vs t0, CD4\n                      <jats:sup>+<\/jats:sup>\n                      CD38\n                      <jats:sup>+<\/jats:sup>\n                      HLA-DR\n                      <jats:sup>+<\/jats:sup>\n                      (percentage of CD4\n                      <jats:sup>+<\/jats:sup>\n                      T lymphocytes), 2.7 (1.7-6.3) vs 9.7 (2.8-18.5), p=0.047; CD8\n                      <jats:sup>+<\/jats:sup>\n                      CD38\n                      <jats:sup>+<\/jats:sup>\n                      HLA-DR\n                      <jats:sup>+<\/jats:sup>\n                      (percentage of CD8\n                      <jats:sup>+<\/jats:sup>\n                      T lymphocytes), 6.5 (3.7-15.5) vs 19.0 (12.0-31.1), p=0.086].\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Untreated PLWH show a dysbiotic signature, characterized by enrichment of SCFA-producers. Compared to controls, the fecal microbiota of PLWH after 6 months of ART (t6) continued to show differences characterized by a predominance of\n                      <jats:italic>Alloprevotella<\/jats:italic>\n                      and\n                      <jats:italic>Succinivibrio<\/jats:italic>\n                      , among others, and continued elevations in intestinal injury, bacterial translocation, and inflammatory\/immune activation markers, underscoring the incomplete normalization of gut-immune homeostasis.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcimb.2026.1853799","type":"journal-article","created":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T04:24:45Z","timestamp":1785126285000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Effect of antiretroviral therapy on gut microbiota, immune activation, and inflammatory markers in newly diagnosed HIV 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