title: [Combined infection with HTLV-1 and Strongyloides stercoralis].
abstract: Infection of carriers of strongyloides by the human oncogenic retrovirus HTLV-1 significantly augments the number of larval parasites in the stools and impairs the action of anti-helminthic agents, resulting in an increase in immediate and longer term failure of therapy. The proliferation of cytokine type 1 secreting lymphocytes, the preferred target for viral infection, shifts the Th1/Th2 balance in favour of a Th1 response with a consequent increase in the production of gamma interferon (INF-γ). In addition to other effects, this causes a decrease in the secretion of cytokines IL-4, IL-5 and IL-13, which results in substantial reduction in total and specific IgE; failure of activation of eosinophils or stagnation in or reduction of their numbers; and an increased risk of development of a severe form of strongyloidiasis. This risk is clearly correlated with the level of anti-HTLV-1 antibodies and the amplitude of the proviral load of peripheral lymphocytes. The polyclonal expansion of infected CD4 cells might be partly due to the activation of the IL-2/IL-2R system by parasite antigens together with the action of the virus type 1 Tax protein. The fact that adult T cell leukaemia arises significantly earlier and more often in individuals with combined infection is an argument in favour of the parasite's role as a leukaemogenic co-factor. In practice it is, therefore, appropriate to initiate all available measures to eliminate parasites from co-infected hosts although this does present difficulties, and one should not reject the possibility of a diagnosis of strongyloidiasis in the absence of hypereosinophilia. In all cases of chronic strongyloidiasis without hypereosinophilia, co-infection with HTLV-1 should be looked for routinely. The same applies to carriers of strongyloides with repeated treatment failures. Finally, corticosteroids and immunosuppressants should be used only with care in HTLV-1-positive patients who seem not to be co-infected, even if they have received precautionary therapy.
authors.affiliation: Faculté de médecine Descartes-Necker, Université Paris-V-René-Descartes, Paris, France. pays@necker.fr
authors.forename: J-F
authors.initials: JF
authors.lastname: Pays
mesh_terms: D000818:Animals; D000871:Anthelmintics / Q000627:therapeutic use; D003043:Cocarcinogenesis; D015897:Comorbidity; D018450:Disease Progression; D004351:Drug Resistance; D004804:Eosinophils / Q000502:physiology; D015490:HTLV-I Infections / Q000150:complications* / Q000453:epidemiology / Q000276:immunology; D006790:Host-Parasite Interactions / Q000276:immunology; D006801:Humans; D007073:Immunoglobulin E / Q000276:immunology; D007814:Larva; D015459:Leukemia-Lymphoma, Adult T-Cell / Q000209:etiology; D008018:Life Cycle Stages; D008954:Models, Biological; D009894:Opportunistic Infections / Q000469:parasitology; D015995:Prevalence; D017171:Strongyloides stercoralis / Q000254:growth & development / Q000502:physiology*; D013322:Strongyloidiasis / Q000150:complications* / Q000188:drug therapy / Q000453:epidemiology / Q000276:immunology; D009626:Terminology as Topic; D058408:Th1-Th2 Balance
chemical_list: D000871:Anthelmintics; D007073:Immunoglobulin E