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

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.

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.