Rifaximin has a Marginal Impact on Microbial Translocation, T-cell Activation and Inflammation in HIV-Positive Immune Non-responders to Antiretroviral Therapy – ACTG A5286

Abstract

In immune nonresponders to ART, rifaximin minimally affected microbial translocation and CD8(+)T-cell activation. Trial registration number. NCT01466595.

Reduced Levels of D-dimer and Changes in Gut Microbiota Composition After Probiotic Intervention in HIV-Infected Individuals on Stable ART

“…However, we could not demonstrate any significant effect on microbial translocation assessed by plasma LPS or sCD14 analyses. This is in line with most recent studies targeting the intestinal microbiota, including intervention with the probiotic/prebiotic combination given to SIV-infected macaques, 26 the LPS-binding agent Sevelamer, 47 the nonabsorbable antibiotic Rifaximin, 48 and the fungus S. boulardii, 46 showing no reduction in LPS or sCD14 levels.…”

Stimulation of PBMC and Monocyte-Derived Macrophages via Toll-Like Receptor Activates Innate Immune Pathways in HIV-Infected Patients on Virally Suppressive Combination Antiretroviral Therapy

“…In this view, our research may partially facilitate an explanation of why rifaximin or sevelamer, by antagonizing microbial bioproducts in the systemic circulation, may not lower T-cell activation in HIV-infected humans (75, 76), despite the intriguing results obtained in the animal model (77). The research may also suggest the need for a more comprehensive elucidation of the role of the TLR system in promoting HIV-driven immune hyperactivation.…”

Impaired gut junctional complexes feature late-treated individuals with suboptimal CD4+ T-cell recovery upon virologically suppressive combination antiretroviral therapy

“…cART intensification [35,39,40,42,43] may result in the inefficient concentration of antiretrovirals in the gut [72]; IL-7 immuneadjuvant therapy may contribute to replenishment of the HIV reservoir rather than its reduction [41,73]; further, rifaximin may not result in the effective control of microbial translocation because of the lasting damage of the gastrointestinal tract [44].…”

“…Further, up to 30% of treated patients fail to recover peripheral CD4 þ [immunological nonresponders (INR)] [35], particularly those starting cART late in the course of disease, with severe CD4 þ depletion. This particular outcome has been associated with a high risk of clinical events and death [36][37][38] as well as poor response to experimental treatments [39][40][41][42][43][44].…”