Clinical and immunological consequences of human T cell leukemia virus type-I and Schistosoma mansoni co-infection

Abstract

Human T cell leukemia virus type-I (HTLV-I) infection is associated with spontaneous T cell activation and uncontrolled lymphocyte proliferation. An exacerbated type-1 immune response with production of pro-inflammatory cytokines (interferon-γ and tumor necrosis factor-α) is significantly higher in patients with myelopathy associated to HTLV-I than in HTLV-I asymptomatic carriers. In contrast with HTLV-I, a chronic Schistosoma mansoni infection is associated with a type-2 immune response with high levels of interleukin (IL-4, IL-5, and IL-10) and low levels of IFN-γ. In this study, clinical and immunological consequences of the HTLV-I and S. mansoni infection were evaluated. The immune response in patients with schistosomiasis co-infected with HTLV-I showed low levels of IL-5 (p < 0.05) in peripheral blood mononuclear cells cultures stimulated with S. mansoni antigen (SWAP) and decreased SWAP-specific IgE levels when compared with patients with only schistosomiasis (p < 0.05). Liver fibrosis was mild in all HTLV-I co-infected patients. Immunological response was also compared in individuals who had only HTLV-I infection with those who were co-infected with HTLV-I and helminths (S. mansoni and Strongyloides stercoralis). In patients HTLV-I positive co-infected with helminths the IFN-γ levels were lower than in individuals who had only HTLV-I. Moreover, there were fewer cells expressing IFN-γ and more cells expressing IL-10 in individuals co-infected with HTLV-I and helminths. These dates indicate that HTLV-I infection decrease type 2-response and IgE synthesis and are inversely associated with the development of liver fibrosis. Moreover, helminths may protect HTLV-I infected patients to produce large quantities of pro-inflammatory cytokines such as IFN-γ.

Effects of schistosomes on host anti-viral immune response and the acquisition, virulence, and prevention of viral infections: A systematic review

“…In two studies, the addition of S. mansoni antigens to PBMC cultures from HTLV-1-infected adults caused increased IL-10 and decreased IFN-γ and CXCL9, important for Th1 cell recruitment [125,126]. Another reported decreased IFN-γ and increased IL-10 in unstimulated PBMC cultures of adults with HTLV-1-helminth co-infection versus with HTLV-1 alone [127], as well as decreased HTLV-1 proviral load in PBMCs of those with coinfection [124]. These data fit with one study's clinical documentation of schistosome or strongyloides infections seven-fold more frequently in HTLV-1 disease carriers than in HTLV-1 infected persons who developed tropical spastic paralysis [124], suggesting that decreased Th1 and increased T regulatory could prevent the development of inflammatory paralysis.…”

Clinical and immunological features of patients with atopy and concomitant HTLV-1 infection

“…In addition to adult T-cell leukemia/lymphoma (ATLL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), patients may present an overactive bladder, sicca syndrome, artropathy, uveitis, and periodontal disease (1)(2)(3). Additionally, HTLV-1 infection may influence the immune response to other pathogens, increasing susceptibility and modifying the clinical manifestation of strongyloidiasis (4,5), tuberculosis (6,7), schistosomiasis (8), and scabies (9). The pathology related to HTLV-1 infection is associated with an exaggerated and inappropriately modulated immune response, and a high proviral load (10).…”

Rinite crônica em portadores do HTLV-1: estudo histopatológico

“…On type 2 immune response, seen in allergic inflammation, there is increased production of IL-4, IL-5, and IL-13 14 . Type 1 and type 2 immune response may be mutually impacted both by contra-regulation and synergy 15 .…”