Abstract Body

HIV alters gastrointestinal (GI) tract permeability, GI lymphoid tissue structure and function, contributing to systemic inflammation. In inflammatory bowel diseases, probiotics can resolve gastrointestinal symptoms and reduce local and systemic inflammation. In this trial, we evaluated whether the probiotic Visbiome Extra Strength (ES) reduced measures of systemic inflammation in persons with HIV (PWH).

 

A5350, a phase II, randomized, double-blind, two-arm, placebo-controlled study, evaluated changes in soluble inflammatory markers after 24 weeks of probiotic Visbiome ES, and the safety/ tolerability in PWH on antiretroviral therapy (ART). Primary endpoint was change in sCD14 levels; secondary measures included D-dimer, Kynurenine to Tryptophan (KT) ratio, CD4 count, & CD4/CD8 ratio. Mean changes were compared between arms with a 2-sample t-test. Per-protocol analysis included all randomized participants with baseline & week 25/26 sCD14 measurements, remained on study product through week 26 with >50% adherence, no use of prohibited medications, without confirmed virologic failure, and did not experience inflammatory conditions, receive vaccines, or have concurrent illness.

 

Overall, 93 participants (46 placebo, 47 Visbiome ES) enrolled; 86% men, 55% white, 42% black, 20% Hispanic/Latino; median (Q1, Q3) age was 51 (45, 56) years, BMI was 27.1 (24.2, 30.7) kg/m2, CD4 count was 712 (542, 893) cells/mm3 and 99% had HIV-1 RNA <40 copies/mL; one participant had 48 copies/mL. Overall, 25 participants reported adverse events: (8 [19%] placebo; 17 [36%] Visbiome ES) (p=0.098). Excluding 19 participants who did not complete study treatment and one virologic failure, 73 participants (31 placebo; 42 Visbiome ES) remained in the per-protocol population. The mean change (95% CI) in sCD14 from baseline to week 25/26 was 92.3 (-48.5, 233) ug/L in the placebo arm and 41.0 (-94.1, 176.2) ug/L in the Visbiome ES arm, but these changes were not statistically different (p=0.60). Similarly, there were no significant differences in changes in D-dimer, KT ratio, CD4 cell counts, CD4/CD8 ratio between the arms.

 

Visbiome ES was safe and well tolerated among this cohort. No significant effect of Visbiome ES on systemic inflammatory markers was identified. While high loss to follow up in the placebo arm limits the strength of our conclusions, these results do not support Visbiome ES as a viable strategy to reduce systemic inflammation in suppressed PWH with preserved CD4 counts.