Strongyloides Stercoralis as Candidate Co-Factor for HTLV-I-Induced Leukaemogenesis

Yamaguchi, Kazunari; Matutes, Estella; Catovsky, Daniel; Galton, D. A. G.; Nakada, Kiyonobu; Takatsuki, Kiyoshi

doi:10.1016/s0140-6736(87)92752-8

Cited by 61 publications

(27 citation statements)

References 4 publications

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“…In such context, the increased infected T cell proliferation associated with Ss infection is thought to increase the frequency of acquired T cell somatic mutations leading to malignant transformation. Therefore, present results help explain why the latency period of ATLL is signi®cantly shortened in patients with strongyloidiasis (Cleghorn et al, 1995;Plumelle et al, 1997;Yamaguchi et al, 1987).…”

Section: Discussionsupporting

confidence: 54%

“…By contrast, Southern-blotting, which has a sensitivity of about 1/20, failed to detect any signal in HTLV-1 infected individuals without strongyloidiasis (Chen et al, 1995;Nakada et al, 1987;Yamaguchi et al, 1988). In addition, Ss has been found to signi®cantly shorten the incubation period of ATLL, which occurs 30 years earlier in HTLV-1 individuals with strongyloidiasis than in other HTLV-1 asymptomatic carriers (Cleghorn et al, 1995;Plumelle et al, 1997;Pombo de Oliveira et al, 1995;Yamaguchi et al, 1987). Indeed, a greater exposure to infectious agents including Ss has been proposed to explain the earlier onset of ATLL in Caribbean/African patients when compared to Japanese patients .…”

Section: Introductionmentioning

confidence: 91%

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High circulating proviral load with oligoclonal expansion of HTLV-1 bearing T cells in HTLV-1 carriers with strongyloidiasis

et al. 2000

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Adult T cell leukemia (ATLL) develops in 3 ± 5% of HTLV-1 carriers after a long period of latency during which a persistent polyclonal expansion of HTLV-1 infected lymphocytes is observed in all individuals. This incubation period is signi®cantly shortened in HTLV-1 carrier with Strongyloides stercoralis (Ss) infection, suggesting that Ss could be a cofactor of ATLL. As an increased T cell proliferation at the asymptomatic stage of HTLV-1 infection could increase the risk of malignant transformation, the e ect of Ss infection on infected T lymphocytes was assessed in vivo in HTLV-1 asymptomatic carriers. After real-time quantitative PCR, the mean circulating HTLV-1 proviral load was more than ®ve times higher in HTLV-1 carriers with stongyloidiasis than in HTLV-1+ individuals without Ss infection (P50.009). This increased proviral load was found to result from the extensive proliferation of a restricted number of infected clones, i.e. from oligoclonal expansion, as evidenced by the semiquantitative ampli®-cation of HTLV-1¯anking sequences. The positive e ect of Ss on clonal expansion was reversible under e ective treatment of strongyloidiasis in one patient with parasitological cure whereas no signi®cant modi®cation of the HTLV-1 replication pattern was observed in an additional case with strongyloidiasis treatment failure. Therefore, Ss stimulates the oligoclonal proliferation of HTLV-1 infected cells in HTLV-1 asymptomatic carriers in vivo. This is thought to account for the shortened period of latency observed in ATLL patients with strongyloidiasis. Oncogene (2000) 19, 4954 ± 4960.

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Section: Discussionsupporting

confidence: 54%

Section: Introductionmentioning

confidence: 91%

High circulating proviral load with oligoclonal expansion of HTLV-1 bearing T cells in HTLV-1 carriers with strongyloidiasis

et al. 2000

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“…Several cycles of transient active proliferation combined with chromosomal instability may be required for a clonal selection and the development of adult T-cell leukemia. In support of such a model, a high frequency of T-cell clonal expansion has been associated with chronic antigenic stimulation in carriers of S. stercoralis [122,123], and a higher frequency of leukemia has been reported in individuals carrying this parasite [124][125][126].…”

Section: Molecular Pathogenesismentioning

confidence: 86%

Current views in HTLV-I-associated adult T-cell leukemia/lymphoma

Nicot

2005

Am. J. Hematol.

104

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Epidemiological studies have demonstrated that the relative percentage of malignant lymphoid proliferations varies widely according to geographical location and ethnic populations. HTLV-I is the etiological agent of adult T-cell leukemia/lymphoma (ATLL) and is also associated with cutaneous T-cell lymphoma (CTCL). However, a definite role of HTLV-I in mycosis fungoides (MF) and/or Sezary syndrome (SS) remains controversial. While most HTLV-I-infected individuals remain asymptomatic carriers, 1-5% will develop ATLL, an invariably fatal expansion of virus-infected CD4 + T cells. This low incidence and the long latency period preceding occurrence of the disease suggest that additional factors are involved in development of ATLL. In this review, diagnosis, clinical features, and molecular pathogenesis of HTLV-I are discussed. Am.

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“…38 This latent or preleukemic phase is reported to be up to 30 years shorter in HTLV-1 carriers who are coinfected with Strongyloides than in other HTLV-1-infected people. [39][40][41][42] Monoclonal proliferation of the HTLV-1-infected cells has been shown to occur in coinfected patients but not in asymptomatic HTLV-1 carriers who do not have strongyloidiasis. 43,44 Furthermore, the results of a recent study have shown that the Strongyloides antigen is implicated in T-cell proliferation and ultimately accelerates leukemogenesis.…”

Section: Risk Factors For Disseminationmentioning

confidence: 99%

Complicated and fatal Strongyloides infection in Canadians: risk factors, diagnosis and management

Lim¹

2004

Canadian Medical Association Journal

159

173

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STRONGYLOIDIASIS, WHICH IS CAUSED by the nematode Strongyloides stercoralis, is a common and persistent infection, particularly in developing countries. In the setting of compromised cellular immunity, it can result in fulminant dissemination with case-fatality rates of over 70%. The majority of new Canadian immigrants come from countries where Strongyloides is highly endemic; therefore, the burden of Strongyloides may be underappreciated in Canada. Because early diagnosis and therapy can have a marked impact on disease outcome, screening for this infection should be considered mandatory for patients who have a history of travel or residence in a disease-endemic area and risk factors for disseminated disease (e.g., corticosteroid use and human Tlymphotropic virus type I infection).

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Strongyloides Stercoralis as Candidate Co-Factor for HTLV-I-Induced Leukaemogenesis

Cited by 61 publications

References 4 publications

High circulating proviral load with oligoclonal expansion of HTLV-1 bearing T cells in HTLV-1 carriers with strongyloidiasis

High circulating proviral load with oligoclonal expansion of HTLV-1 bearing T cells in HTLV-1 carriers with strongyloidiasis

Current views in HTLV-I-associated adult T-cell leukemia/lymphoma

Complicated and fatal Strongyloides infection in Canadians: risk factors, diagnosis and management

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