Combined infection with HTLV-1 and Strongyloides stercoralis
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 cytokin...
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description | 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. |
doi_str_mv | 10.1007/s13149-011-0175-z |
format | Article |
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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.</description><identifier>ISSN: 0037-9085</identifier><identifier>DOI: 10.1007/s13149-011-0175-z</identifier><identifier>PMID: 21800110</identifier><language>fre</language><publisher>France</publisher><subject>Animals ; Anthelmintics - therapeutic use ; Cocarcinogenesis ; Comorbidity ; Disease Progression ; Drug Resistance ; Eosinophils - physiology ; Host-Parasite Interactions - immunology ; HTLV-I Infections - complications ; HTLV-I Infections - epidemiology ; HTLV-I Infections - immunology ; Humans ; Immunoglobulin E - immunology ; Larva ; Leukemia-Lymphoma, Adult T-Cell - etiology ; Life Cycle Stages ; Models, Biological ; Opportunistic Infections - parasitology ; Prevalence ; Strongyloides stercoralis - growth & development ; Strongyloides stercoralis - physiology ; Strongyloidiasis - complications ; Strongyloidiasis - drug therapy ; Strongyloidiasis - epidemiology ; Strongyloidiasis - immunology ; Terminology as Topic ; Th1-Th2 Balance</subject><ispartof>Bulletin de la Societe de pathologie exotique (1990), 2011-08, Vol.104 (3), p.188-199</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21800110$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pays, J-F</creatorcontrib><title>Combined infection with HTLV-1 and Strongyloides stercoralis</title><title>Bulletin de la Societe de pathologie exotique (1990)</title><addtitle>Bull Soc Pathol Exot</addtitle><description>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.</description><subject>Animals</subject><subject>Anthelmintics - therapeutic use</subject><subject>Cocarcinogenesis</subject><subject>Comorbidity</subject><subject>Disease Progression</subject><subject>Drug Resistance</subject><subject>Eosinophils - physiology</subject><subject>Host-Parasite Interactions - immunology</subject><subject>HTLV-I Infections - complications</subject><subject>HTLV-I Infections - epidemiology</subject><subject>HTLV-I Infections - immunology</subject><subject>Humans</subject><subject>Immunoglobulin E - immunology</subject><subject>Larva</subject><subject>Leukemia-Lymphoma, Adult T-Cell - etiology</subject><subject>Life Cycle Stages</subject><subject>Models, Biological</subject><subject>Opportunistic Infections - parasitology</subject><subject>Prevalence</subject><subject>Strongyloides stercoralis - growth & development</subject><subject>Strongyloides stercoralis - physiology</subject><subject>Strongyloidiasis - complications</subject><subject>Strongyloidiasis - drug therapy</subject><subject>Strongyloidiasis - epidemiology</subject><subject>Strongyloidiasis - immunology</subject><subject>Terminology as Topic</subject><subject>Th1-Th2 Balance</subject><issn>0037-9085</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1j01LxDAYhHNQ3GXdH-BFevMUfd-2-Sh4kUV3hYIHi9eSNIlG2qY2LbL-eguuh2HmgWFgCLlCuEUAcRcxw7yggLhIMPpzRtYAmaAFSLYi2xg_AQAl4sIXZJWiXBBhTe53odO-tybxvbPN5EOffPvpIzlU5RvFRPUmeZ3G0L8f2-CNjUmc7NiEUbU-XpJzp9potyffkOrpsdodaPmyf949lHRgDKgwjGuWF8BZkebg9BJlARahKXjqTJZrkWrA1OXOmVwiF8ANMM2V4ah0tiE3f7PDGL5mG6e687Gxbat6G-ZYSykYcMjSpXl9as66s6YeRt-p8Vj__81-ARfBVKA</recordid><startdate>201108</startdate><enddate>201108</enddate><creator>Pays, J-F</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>201108</creationdate><title>Combined infection with HTLV-1 and Strongyloides stercoralis</title><author>Pays, J-F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p550-7d56b5490659240fb490890e10c962fd34b72b012f4ffd4816706d05b6ad61ab3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>fre</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Anthelmintics - therapeutic use</topic><topic>Cocarcinogenesis</topic><topic>Comorbidity</topic><topic>Disease Progression</topic><topic>Drug Resistance</topic><topic>Eosinophils - physiology</topic><topic>Host-Parasite Interactions - immunology</topic><topic>HTLV-I Infections - complications</topic><topic>HTLV-I Infections - epidemiology</topic><topic>HTLV-I Infections - immunology</topic><topic>Humans</topic><topic>Immunoglobulin E - immunology</topic><topic>Larva</topic><topic>Leukemia-Lymphoma, Adult T-Cell - etiology</topic><topic>Life Cycle Stages</topic><topic>Models, Biological</topic><topic>Opportunistic Infections - parasitology</topic><topic>Prevalence</topic><topic>Strongyloides stercoralis - growth & development</topic><topic>Strongyloides stercoralis - physiology</topic><topic>Strongyloidiasis - complications</topic><topic>Strongyloidiasis - drug therapy</topic><topic>Strongyloidiasis - epidemiology</topic><topic>Strongyloidiasis - immunology</topic><topic>Terminology as Topic</topic><topic>Th1-Th2 Balance</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pays, J-F</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Bulletin de la Societe de pathologie exotique (1990)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pays, J-F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Combined infection with HTLV-1 and Strongyloides stercoralis</atitle><jtitle>Bulletin de la Societe de pathologie exotique (1990)</jtitle><addtitle>Bull Soc Pathol Exot</addtitle><date>2011-08</date><risdate>2011</risdate><volume>104</volume><issue>3</issue><spage>188</spage><epage>199</epage><pages>188-199</pages><issn>0037-9085</issn><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.</abstract><cop>France</cop><pmid>21800110</pmid><doi>10.1007/s13149-011-0175-z</doi><tpages>12</tpages></addata></record> |
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subjects | Animals Anthelmintics - therapeutic use Cocarcinogenesis Comorbidity Disease Progression Drug Resistance Eosinophils - physiology Host-Parasite Interactions - immunology HTLV-I Infections - complications HTLV-I Infections - epidemiology HTLV-I Infections - immunology Humans Immunoglobulin E - immunology Larva Leukemia-Lymphoma, Adult T-Cell - etiology Life Cycle Stages Models, Biological Opportunistic Infections - parasitology Prevalence Strongyloides stercoralis - growth & development Strongyloides stercoralis - physiology Strongyloidiasis - complications Strongyloidiasis - drug therapy Strongyloidiasis - epidemiology Strongyloidiasis - immunology Terminology as Topic Th1-Th2 Balance |
title | Combined infection with HTLV-1 and Strongyloides stercoralis |
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