Résumé
L’infection des porteurs d’anguillules par le rétrovirus humain oncogène HTLV-1 accroît significativement le nombre des larves du parasite présentes dans les selles et interfère avec les anthelminthiques en multipliant le nombre des échecs thérapeutiques immédiats ou à terme. La prolifération des lymphocytes secrétant des cytokines de type 1, cibles préférentielles de l’infection virale, entraîne une bascule de la balance Th1/Th2 en faveur d’une réponse Th1, et donc une production accrue d’interféron gamma (INF-γ). Celle-ci se traduit, entre autres, par le biais de la diminution de la sécrétion des cytokines IL-4, IL-5, IL-13 qu’elle entraîne par une baisse importante des IgE totales et spécifiques, une non-activation, une baisse ou une stagnation du nombre des éosinophiles et un risque accru de voir apparaître une forme grave d’anguillulose. Le taux des anticorps anti-HTLV-1 et l’importance de la charge provirale des lymphocytes périphériques sont apparemment corrélés à ce risque. L’expansion polyclonale des CD4 infectés pourrait être due en partie à l’activation du système IL-2/IL-2R par les antigènes parasitaires, en complément de l’action de la protéine virale Tax. Le fait que la survenue des ATL soit significativement plus précoce et plus fréquente chez les co-infectés est un argument en faveur du rôle joué par le parasite comme cofacteur leucémogène. Il convient donc, en pratique, de tout mettre en oeuvre pour déparasiter les co-infectés, malgré les difficultés que cela représente, et de ne pas refuser l’éventualité diagnostique d’une anguillulose en l’absence d’hyperéosinophilie. Dans tous les cas d’anguillulose chronique sans hyperéosinophilie, la recherche d’une co-infection avec le HTLV-1 devra être systématique, ainsi que chez les porteurs d’anguillules en échec répété de traitement. Les corticoïdes et les immunosuppresseurs, enfin, ne devront être utilisés qu’avec prudence chez les HTLV-1 positifs apparemment non co-infectés, même après traitement de sécurité.
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.
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Pays, J.F. Co-infections HTLV-1-Strongyloides stercoralis . Bull. Soc. Pathol. Exot. 104, 188–199 (2011). https://doi.org/10.1007/s13149-011-0175-z
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DOI: https://doi.org/10.1007/s13149-011-0175-z
Mots clés
- Strongyloides stercoralis
- Strongyloïdose
- Co-infection
- Hyperéosinophilie
- Hyperinfection
- Anguillulose systémique
- HTLV-1
- ATL
- Schistosoma mansoni
- HIV-1
- HAM/TSP