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Background <p>Unwanted weight gain is often reported in people living with HIV (PWH) who start on or switch to integrase strand transfer inhibitors (INSTI). Mechanisms are incompletely understood. An unintended off-target of INSTI might be the gut microbiota.</p> Methods <p>We explored the fecal microbiota of treated aviremic PWH (<i>n</i> = 70) who switched from efavirenz (EFV)- to a bictegravir (BIC)-based regimen. 16S rRNA sequencing, and enzyme-linked immunosorbent assays were used to characterize the fecal microbiota and quantify markers of HIV disease progression. A cohort of high-risk HIV-negative individuals (<i>n</i> = 18) was included to address differential effects of antiretroviral therapy (ART) on the fecal microbiota.</p> Results <p>This real-life cohort was predominantly male (<i>n</i> = 63) and mostly men who have sex with men (<i>n</i> = 40). All PWH were on the same antiretroviral regimen for at least 1 year; the mean time on ART was 10.83 ± 5.530 years and all had undetectable plasma viral loads (&lt; 40 HIV-1 RNA copies/mL). PWH gained a median weight of 3.375&#xa0;kg and the mean percent weight change relative to baseline was 4.32%. Seven (10%) PWH gained significant weight (&gt; 10% relative to baseline). Switching to a BIC-based regimen had contrasting effects. PWH on BIC/FTC/TAF showed decreased microbial translocation (soluble CD14, sCD14), decreased enterocyte damage (intestinal fatty-acid binding protein, I-FABP), and increased alpha diversity (richness and shannon); all indicative of a better restoration of the gut mucosa and microbiota. Conversely, increases in sCD163, monocyte chemoattractant protein 1 (MCP-1) and decreases in adiponectin, markers linked to cardiovascular disease, insulin resistance and adiposity, were unfavorable.</p> Conclusion <p>Our data suggest that INSTI have a less detrimental effect on the gut microbiota compared to EFV-based regimen. The link between weight gain on INSTI and the gut microbiota was not readily apparent.</p>

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Differential effects of switching to integrase strand transfer inhibitors on the gut microbiota and markers of HIV disease progression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月1日

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  • Sandra M. Pinto-Cardoso,
  • Adriana Aguilar-Vargas,
  • Mariana López-Filloy,
  • Monserrat Chávez-Torres,
  • Akio Murakami-Osawara,
  • Olivia Briceño,
  • Karla Romero-Mora,
  • Nadia Rodríguez-Moguel,
  • Gonzalo Salgado Montes de Oca,
  • Santiago Ávila-Ríos,
  • Amy Bethel Peralta-Prado,
  • Andrea Cárdenas Ortega,
  • Elizabeth Ramírez Palacios,
  • Edna Hania Rodriguéz Aguirre,
  • Flor Cano Jiménez,
  • Laura Lorena Jiménez Sánchez,
  • Norma Emilia Mirafuentes Ramón,
  • Juan Ramón Hernández,
  • Daniela Garrido-Rodriguéz

摘要

Background

Unwanted weight gain is often reported in people living with HIV (PWH) who start on or switch to integrase strand transfer inhibitors (INSTI). Mechanisms are incompletely understood. An unintended off-target of INSTI might be the gut microbiota.

Methods

We explored the fecal microbiota of treated aviremic PWH (n = 70) who switched from efavirenz (EFV)- to a bictegravir (BIC)-based regimen. 16S rRNA sequencing, and enzyme-linked immunosorbent assays were used to characterize the fecal microbiota and quantify markers of HIV disease progression. A cohort of high-risk HIV-negative individuals (n = 18) was included to address differential effects of antiretroviral therapy (ART) on the fecal microbiota.

Results

This real-life cohort was predominantly male (n = 63) and mostly men who have sex with men (n = 40). All PWH were on the same antiretroviral regimen for at least 1 year; the mean time on ART was 10.83 ± 5.530 years and all had undetectable plasma viral loads (< 40 HIV-1 RNA copies/mL). PWH gained a median weight of 3.375 kg and the mean percent weight change relative to baseline was 4.32%. Seven (10%) PWH gained significant weight (> 10% relative to baseline). Switching to a BIC-based regimen had contrasting effects. PWH on BIC/FTC/TAF showed decreased microbial translocation (soluble CD14, sCD14), decreased enterocyte damage (intestinal fatty-acid binding protein, I-FABP), and increased alpha diversity (richness and shannon); all indicative of a better restoration of the gut mucosa and microbiota. Conversely, increases in sCD163, monocyte chemoattractant protein 1 (MCP-1) and decreases in adiponectin, markers linked to cardiovascular disease, insulin resistance and adiposity, were unfavorable.

Conclusion

Our data suggest that INSTI have a less detrimental effect on the gut microbiota compared to EFV-based regimen. The link between weight gain on INSTI and the gut microbiota was not readily apparent.