# Helminth Immune Modulation and Invasive Fungal Infections in Sub-Saharan Africa

**Authors:** Luis Fonte, Yaxsier de Armas, Héctor R. Pérez-Gómez, Enrique J. Calderón

PMC · DOI: 10.3390/jof12020160 · 2026-02-23

## TL;DR

This paper explores how helminth infections in sub-Saharan Africa may indirectly and possibly directly contribute to invasive fungal infections through immune modulation and social factors.

## Contribution

The paper introduces a syndemic perspective linking helminth immune modulation to fungal infections in sub-Saharan Africa.

## Key findings

- Helminth infections may impair immune responses to HIV and tuberculosis, indirectly promoting fungal infections.
- Epidemiological patterns suggest helminth immune modulation could directly influence fungal infections in the region.
- A syndemic approach is needed to address the complex interactions of infections and social factors in sub-Saharan Africa.

## Abstract

Sub-Saharan Africa, a region marked by enormous social and health inequalities, has the largest population infected with HIV and Mycobacterium tuberculosis, which are considered the main risk factors for fungal infections. At the same time, sub-Saharan Africa is the region of the world with the highest rates of helminth infections, whose immunomodulatory effects impair the host’s immune responses to other microorganisms, including HIV and M. tuberculosis. Through this indirect way, helminth immune modulation could be another syndemic factor influencing the development of fungal infections. However, some epidemiological peculiarities of five fungal diseases in sub-Saharan Africa, which we analyze in this paper, suggest that the influence of helminth immune modulation on the development of fungal infections there could also be direct. In light of the knowledge of all those interactions, any healthcare and epidemiological approach to Invasive Fungal Infections in sub-Saharan Africa should be carried out from a syndemic perspective that takes into account the ways in which social environments contribute to the clustering of infections, the pathways through which infecting microorganisms could interact biologically in each individual, influencing the development and evolution of the disease in course, and the ways in which those interactions complicate diagnosis, treatment, and control.

## Full-text entities

- **Genes:** IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, RAG1 (recombination activating 1) [NCBI Gene 5896] {aka RAG-1, RNF74}, IL12B (interleukin 12B) [NCBI Gene 3593] {aka CLMF, CLMF2, IL-12B, IMD28, IMD29, NKSF}, FOXP3 (forkhead box P3) [NCBI Gene 50943] {aka AIID, DIETER, IPEX, JM2, PIDX, XPID}, IL23A (interleukin 23 subunit alpha) [NCBI Gene 51561] {aka IL-23, IL-23A, IL23P19, P19, SGRF}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, IL5 (interleukin 5) [NCBI Gene 3567] {aka EDF, IL-5, TRF}, IL13 (interleukin 13) [NCBI Gene 3596] {aka IL-13, P600}, CD4 (CD4 molecule) [NCBI Gene 920] {aka CD4mut, IMD79, Leu-3, OKT4D, T4}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, IL4 (interleukin 4) [NCBI Gene 3565] {aka BCGF-1, BCGF1, BSF-1, BSF1, IL-4}
- **Diseases:** injury to (MESH:D014947), inflammatory (MESH:D007249), PcP (MESH:D011020), asthmatic (MESH:D013224), respiratory disease (MESH:D012140), skin lesions (MESH:D012871), soil-transmitted helminths infections (MESH:D012749), talaromycosis (MESH:C000656865), lung disease (MESH:D008171), cancer (MESH:D009369), opportunistic infection (MESH:D009894), schistosomiasis (MESH:D012552), asthma (MESH:D001249), AIDS (MESH:D000163), cryptococcal infection (MESH:D016919), pulmonary inflammatory (MESH:D016726), bacterial pneumonia (MESH:D018410), Cryptococcosis (MESH:D003453), Histoplasma infection (MESH:D006660), malnutrition (MESH:D044342), neutropenia (MESH:D009503), immunodeficiencies (MESH:D007153), death (MESH:D003643), P. jirovecii infection (MESH:D016720), helminth infections (MESH:D007239), COVID-19 (MESH:D000086382), ABPA (MESH:D001229), IA (MESH:D055744), mycosis (MESH:D015821), M. tuberculosis (MESH:D014376), allergic disease (MESH:D004342), malaria (MESH:D008288), HIV (MESH:D015658), IFIs (MESH:D000072742), fungal disease (MESH:D009181), aspergillosis (MESH:D001228), Emergomycosis (MESH:C000656884), infectious diseases (MESH:D003141)
- **Chemicals:** rituximab (MESH:D000069283), cotrimoxazole (MESH:D015662)
- **Species:** Aspergillus fumigatus (species) [taxon 746128], Pneumocystis (genus) [taxon 4753], Mus musculus (house mouse, species) [taxon 10090], Saccharomyces cerevisiae (baker's yeast, species) [taxon 4932], Nippostrongylus brasiliensis (species) [taxon 27835], Emergomyces pasteurianus (species) [taxon 1955774], Pneumocystis jirovecii (species) [taxon 42068], Human immunodeficiency virus 1 (no rank) [taxon 11676], Histoplasma capsulatum (species) [taxon 5037], Fungi (kingdom) [taxon 4751], Mycobacteriales (order) [taxon 85007], Human immunodeficiency virus (species) [taxon 12721], Mycobacterium tuberculosis (species) [taxon 1773], Emergomyces (genus) [taxon 1955773], Homo sapiens (human, species) [taxon 9606], Cryptococcus (genus) [taxon 79213]

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Source: https://tomesphere.com/paper/PMC12941898