Epidemiological and clinical interaction between HTLV‐1 and Strongyloides stercoralis

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Abstract
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-gamma 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.