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Published on: December 18, 2017
Altered Intestinal Permeability and Fungal Translocation in Ugandan Children With Human Immunodeficiency Virus
Sahera Dirajlal-Fargo1,2,3, Vanessa El-Kamari3, Lukasz Weiner2
1University Hospitals Cleveland Medical Center, Columbus.
Insights
Children with perinatally acquired HIV (PHIV) show increased gut permeability and fungal translocation, even with suppressed viral loads. This gut dysbiosis may contribute to persistent inflammation and long-term health issues in PHIV.
Area of Science:
- Pediatric Infectious Diseases
- Immunology
- Gastroenterology
Background:
- Children with perinatally acquired HIV (PHIV) experience lifelong exposure to HIV and antiretroviral therapy (ART).
- The interplay between gut integrity, microbial translocation, and inflammation in PHIV is not well understood.
- Understanding these factors is crucial for managing long-term health outcomes in PHIV.
Purpose of the Study:
- To investigate gut integrity, microbial translocation, and systemic inflammation in children with PHIV.
- To compare these markers between PHIV, HIV-exposed but uninfected (HEU), and HIV-unexposed and uninfected (HUU) children.
- To explore correlations between gut biomarkers and systemic inflammation in PHIV.
Main Methods:
- A cross-sectional study involving 57 PHIV, 59 HEU, and 56 HUU children aged 2-10 years in Uganda.
- Measurement of systemic inflammation, monocyte activation, and gut integrity markers.
- Statistical analysis using Kruskal-Wallis tests and Spearman correlation.
Main Results:
- PHIV children exhibited higher levels of soluble CD14 (sCD14), beta-D-glucan (BDG), and zonulin, indicating altered gut permeability and fungal translocation.
- Intestinal fatty acid binding protein (I-FABP) and lipopolysaccharide binding protein (LBP) did not differ significantly between groups.
- Breastfeeding in PHIV was associated with higher levels of sCD163 and IL-6, and gut biomarkers correlated with systemic inflammation markers in this subgroup.
Conclusions:
- Despite viral suppression, PHIV children demonstrate impaired gut permeability and fungal translocation.
- Intestinal damage and subsequent microbial translocation in PHIV may contribute to chronic inflammation.
- These findings highlight potential mechanisms underlying end-organ damage in adults with PHIV.
Background:
Children with perinatally acquired human immunodeficiency virus (HIV; PHIVs) face a lifelong cumulative exposure to HIV and antiretroviral therapy (ART). The relationship between gut integrity, microbial translocation, and inflammation in PHIV is poorly understood.
Methods:
This is a cross-sectional study in 57 PHIVs, 59 HIV-exposed but uninfected children, and 56 HIV-unexposed and -uninfected children aged 2-10 years old in Uganda. PHIVs were on stable ART with HIV-1 RNA <400 copies/mL. We measured markers of systemic inflammation, monocyte activation, and gut integrity. Kruskal-Wallis tests were used to compare markers by group and the Spearman correlation was used to assess correlations between biomarkers.
Results:
The mean age of all participants was 7 years and 55% were girls. Among PHIVs, the mean CD4 % was 34%, 93% had a viral load ≤20 copies/mL, and 79% were on a nonnucleoside reverse transcriptase inhibitor regimen. Soluble cluster of differentiation 14 (sCD14), beta-D-glucan (BDG), and zonulin were higher in the PHIV group (P ≤ .01). Intestinal fatty acid binding protein (I-FABP) and lipopolysaccharide binding protein (LBP) did not differ between groups (P > .05). Among PHIVs who were breastfed, levels of sCD163 and interleukin 6 (IL6) were higher than levels in PHIV who were not breastfed (P < .05). Additionally, in PHIVs with a history of breastfeeding, sCD14, BDG, LBP, zonulin, and I-FABP correlated with several markers of systemic inflammation, including high-sensitivity C-reactive protein, IL6, d-dimer, and systemic tumor necrosis factor receptors I and II (P ≤ .05).
Conclusions:
Despite viral suppression, PHIVs have evidence of altered gut permeability and fungal translocation. Intestinal damage and the resultant bacterial and fungal translocations in PHIVs may play a role in the persistent inflammation that leads to many end-organ diseases in adults.Despite viral suppression, children with perinatally acquired human immunodeficiency virus (HIV) in Uganda have evidence of alterations in intestinal permeability and fungal translocation, compared to HIV-exposed but uninfected and HIV-unexposed children, which may play a role in HIV-associated chronic inflammation.
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