Impact of Intestinal Parasitic Infections on Gut Epithelial Barrier and Inflammation among Foreign-Born Persons Living with HIV.

Abstract

Increased enterocyte turnover, microbial translocation, and systemic inflammation have been demonstrated to serve as predictors of morbidity and mortality in people with HIV (PWH) receiving antiretroviral therapy. Both HIV and intestinal parasitic infections cause gut damage and increased microbial translocation. A prospective cohort study of foreign-born PWH with undetectable HIV RNA (<20 copies/mL) with and without intestinal parasitic coinfection was conducted. Biomarkers of enterocyte turnover (intestinal fatty acid binding protein [IFABP]), microbial translocation (soluble cluster of differentiation [CD]14), and systemic inflammation (soluble CD163) were measured. Stool parasite real-time quantitative polymerase chain reaction (qPCR) testing and Strongyloides stercoralis recombinant IgG ELISA (Strongy IgG) were used to diagnose parasitic infection. Of the 52 participants, 14 (27%) tested positive for infection with Strongyloides stercoralis by Strongy IgG, and five (11%) of the 45 participants who provided stool samples tested positive for a parasitic infection (not including Blastocystis) by stool qPCR. The median soluble CD (sCD)14 level in PWH with positive Strongy IgG results was significantly higher than in those with negative Strongy IgG results (1.69 µg/mL versus 1.48 µg/mL; P = 0.03). Soluble CD163 and IFABP levels did not differ significantly between groups. Participants with positive Strongy IgG results demonstrated an increase of 63.4 CD4+ T cells/µL (-161 to 195) after 316.2 (87 to 625) days after strongyloidiasis treatment (P = 0.035). Participants with both HIV and an intestinal parasite infection exhibited increased levels of sCD14, a marker of microbial translocation that has been shown to be an independent predictor of mortality in PWH, compared with those without parasitic infections. Interestingly, CD4+ T cells increased after strongyloidiasis treatment.