Contribution of Schistosoma mansoni to systemic inflammation and microbial translocation among people with HIV in Zambia. (14th July 2021)

• Record Type: Journal Article
• Authors: Furch, Briana D; Mwakamui, Simutanyi; Sianongo, Sandie; Zyambo, Kanekwa; Heimburger, Douglas C; Koethe, John R; Kelly, Paul
• Is Part Of: Transactions of the Royal Society of Tropical Medicine and Hygiene. Volume 116:Number 2(2022)
• Page Start: 179
• Page End: 186
• Publication Date: 2021-07-14
• Subjects: HIV -- inflammation -- microbial translocation -- Schistosomiasis -- Zambia; Tropical medicine -- Periodicals; 616.9883
• DOI: 10.1093/trstmh/trab103
• Languages: English
• ISSNs: 0035-9203

Abstract

Abstract: Background: Schistosoma mansoni is hyperendemic in many rural areas of Zambia where up to 77% of people are positive for infection via serologic evaluation. Zambia also has a high prevalence of HIV infection. Individually, S. mansoni and HIV infection impair gastrointestinal barrier integrity and induce inflammation, but the effects of coinfection are not well understood. We set out to test the hypothesis that HIV would exacerbate intestinal barrier failure in patients with S. mansoni infection. Methods: Adults attending medical outpatient clinics in Kaoma, Western Province, Zambia, were enrolled in a case-control study to determine the relative contributions of schistosomiasis and HIV to microbial translocation (measured as soluble CD14 [sCD14] and lipopolysaccharide binding protein [LBP]) and inflammation (measured as CRP). Results: Among 152 adults evaluated, 74 (49%) were HIV-seropositive, 45 (29%) were shedding schistosome ova (Kato-Katz), 120 (81%) were seropositive for schistosome antibodies (i.e. prior or current infection, with or without egg shedding) and 16 (11%) were HIV/schistosome coinfected (defined by Kato-Katz). HIV infection was associated with higher circulating sCD14 concentrations (p=0.003 by Kruskal–Wallis test), but schistosomiasis was not. HIV infection was associated with greater exposure to schistosomes assessed serologically (OR=2.48, 95% CI 1.05 to 5.86; p=0.03), but reduced likelihood of egg shedding (OR 0.47, 95% CI 0.21 to 1.01; p=0.03). Conclusions: There was no evidence for a compounding or synergistic effect of coinfection on microbial translocation that appeared to be correlated with HIV infection. Further studies are needed to understand how the increase in LBP secondary to HIV infection may decrease schistosome egg excretion in coinfected individuals.