Epidemiological and clinical interaction between HTLV‐1 and Strongyloides stercoralis

Abstract

SUMMARY: Strongyloides stercoralis is the most common human parasitic nematode that is able to complete a life cycle and proliferate within its host. The majority of patients with strongyloidiasis have an asymptomatic infection or mild disease. However, when autoinfection occurs, a high number of infecting larvae can gain access to the bloodstream by penetrating the colonic mucosa leading to a severe hyperinfection and the development of disseminated strongyloidiasis. The human T cell lymphotropic virus type 1 (HTLV‐1) predominantly infects T cells and induces spontaneous lymphocyte proliferation and secretion of high levels of type 1 cytokines. Strongyloides stercoralis patients with HTLV‐1 co‐infection have a modified immunological responses against parasite antigens and co‐infection has clinical implications for strongyloidiasis. The high production of IFN‐γ observed in patients co‐infected with HTLV‐1 and Strongyloides stercoralis decreases the production of IL‐4, IL‐5, IL‐13 and IgE, molecules that participate in the host defence mechanism against helminths. Moreover, there is a decrease in the efficacy of treatment of Strongyloides stercoralis in patients co‐infected with HTLV‐1. Alterations in the immune response against Strongyloides stercoralis and the decrease in the efficacy of anti‐parasitic drugs are responsible for the increased prevalence of Strongyloides stercoralis among HTLV‐1 infected subjects and make HTLV‐1 infection the most important risk factor for disseminated strongyloidiasis.