HIV–Malaria Co-infection Is Associated with a Non-additive Pro-inflammatory Shift in the TNF-α/IL-10 Axis: A Comparative Study of Adults in the Niger Delta, Nigeria

Abstract

Aims: To determine whether HIV–malaria co-infection produces an additive (intermediate) or a non-additive (distinct) shift in the plasma TNF-α/IL-10 axis, relative to malaria or HIV infection alone, among adults in the Niger Delta region of Nigeria. Study Design: A hospital-based, descriptive, comparative cross-sectional study. Place and Duration of Study: Central Hospital, Warri, Delta State, Nigeria, together with selected secondary health facilities, from May 2026 to 30 July 2026. Methodology: Seventy adults were recruited by consecutive sampling into each of three groups: malaria only, HIV only, and HIV–malaria co-infection (n = 210). Malaria was confirmed by microscopy and rapid diagnostic testing; only Plasmodium falciparum infection was included, and non-falciparum species were excluded. HIV status was confirmed using the national serial testing algorithm. Plasma TNF-α and IL-10 were quantified by sandwich enzyme-linked immunosorbent assay, and the IL-10/TNF-α ratio was calculated for each participant. Group comparisons used the Kruskal–Wallis test with Bonferroni-corrected pairwise post hoc comparisons. Results: Plasma TNF-α was more than twice as high in co-infection (27.67 ± 9.24 pg/ml) as in malaria only (13.23 ± 3.79 pg/ml) or HIV only (11.20 ± 2.17 pg/ml; P < .001). The IL-10/TNF-α ratio did not differ between the two mono-infected groups (P = .123) but was markedly lower in co-infection (0.76 ± 0.33 versus 2.12 ± 0.90 and 1.87 ± 0.91; P < .001 for both comparisons). For every parameter examined, the co-infection group's value fell outside, rather than between, the range spanned by the two mono-infected groups. Conclusion: HIV–malaria co-infection in this Niger Delta population is associated with a cytokine profile that is qualitatively distinct from, rather than intermediate between, either infection alone, providing Niger Delta-specific empirical support for a non-additive model of co-infection immunopathogenesis.