Spontaneous neutrophil activation in HTLV-1 infected patients

Human T cell lymphotropic Virus type-1 (HTLV-1) induces lymphocyte activation and proliferation, but little is known about the innate immune response due to HTLV-1 infection. We evaluated the percentage of neutrophils that metabolize Nitroblue tetrazolium (NBT) to formazan in HTLV-1 infected subjects and the association between neutrophil activation and IFN-gamma and TNF-alpha levels. Blood was collected from 35 HTLV-1 carriers, from 8 patients with HAM/TSP (HTLV-1- associated myelopathy); 22 healthy individuals were evaluated for spontaneous and lipopolysaccharide (LPS)-stimulated neutrophil activity (reduction of NBT to formazan). The production of IFN-gamma and TNF-alpha by unstimulated mononuclear cells was determined by ELISA. Spontaneous NBT levels, as well as spontaneous IFN-gamma and TNF-alpha production, were significantly higher (p<0.001) in HTLV-1 infected subjects than in healthy individuals. A trend towards a positive correlation was noted, with increasing percentage of NBT positive neutrophils and levels of IFN-gamma. The high IFN-gamma producing HTLV-1 patient group had significantly greater NBT than healthy controls, 43±24 percent and 17±4.8 percent respectively (p< 0.001), while no significant difference was observed between healthy controls and the low IFN-gamma-producing HTLV-1 patient group (30±20 percent). Spontaneous neutrophil activation is another marker of immune perturbation resulting from HTLV-1 infection. In vivo activation of neutrophils observed in HTLV-1 infected subjects is likely to be the same process that causes spontaneous IFN-gamma production, or it may partially result from direct IFN-gamma stimulation.

Atypical clinical presentation of strongyloidiasis in a patient co-infected with human T cell lymphotrophic virus type I.

Alterations in the immunologic response induced by human T cell lymphotrophic virus type I (HTLV-I) predispose the development of disseminated strongyloidiasis. We report a case of an atypical clinical presentation of strongyloidiasis in a patient co-infected with HTLV-I causing scrotal and perineal pain and infertility. Strongyloides stercoralis was found in the analysis of the sperm and specific therapy for strongyloidiasis was associated with disappearance of the symptoms.

Spontaneous neutrophil activation in HTLV-1 infected patients.

Human T cell lymphotropic Virus type-1 (HTLV-1) induces lymphocyte activation and proliferation, but little is known about the innate immune response due to HTLV-1 infection. We evaluated the percentage of neutrophils that metabolize Nitroblue tetrazolium (NBT) to formazan in HTLV-1 infected subjects and the association between neutrophil activation and IFN-gamma and TNF-alpha levels. Blood was collected from 35 HTLV-1 carriers, from 8 patients with HAM/TSP (HTLV-1- associated myelopathy); 22 healthy individuals were evaluated for spontaneous and lipopolysaccharide (LPS)-stimulated neutrophil activity (reduction of NBT to formazan). The production of IFN-gamma and TNF-alpha by unstimulated mononuclear cells was determined by ELISA. Spontaneous NBT levels, as well as spontaneous IFN-gamma and TNF-alpha production, were significantly higher (p<0.001) in HTLV-1 infected subjects than in healthy individuals. A trend towards a positive correlation was noted, with increasing percentage of NBT positive neutrophils and levels of IFN-gamma. The high IFN-gamma producing HTLV-1 patient group had significantly greater NBT than healthy controls, 43+/-24% and 17+/-4.8% respectively (p< 0.001), while no significant difference was observed between healthy controls and the low IFN-gamma-producing HTLV-1 patient group (30+/-20%). Spontaneous neutrophil activation is another marker of immune perturbation resulting from HTLV-1 infection. In vivo activation of neutrophils observed in HTLV-1 infected subjects is likely to be the same process that causes spontaneous IFN-gamma production, or it may partially result from direct IFN-gamma stimulation.

Implicações clínicas e imunológicas da associação entre o HTLV-1 e a estrongiloidíase / Clinical and immunological consequences of the association between HTLV-1 and strongyloidiasis

A estrongiloidíase é uma das mais importantes helmintíases em países tropicais e estudos epidemiológicos têm demonstrado associaçäo desta parasitose com o vírus HTLV-1. Em regiöes onde estes dois agentes säo endêmicos a coinfecçäo pode resultar no desenvolvimento de formas disseminadas da estrongiloidíase assim como em estrongiloidíase recorrente. Enquanto que o vírus HTLV-1 está relacionado com uma alta produçäo de IFN-gama e desvio da resposta imune para o tipo Th1, a proteçäo contra helmintos está associada a uma resposta Th2. Devido a este viés da resposta imune, indivíduos infectados pelo HTLV-1 apresentam reduçäo na produçäo de IL-4, IL-5, IL-13 e IgE, componentes participantes dos mecanismos de defesa contra S. stercoralis. Estas anormalidades constituem a base para a ocorrência de maior freqüência e de formas mais graves da estrongiloidíase em pacientes infectados pelo HTLV-1

[Clinical and immunological consequences of the association between HTLV-1 and strongyloidiasis]. / Implicações clínicas e imunológicas da associação entre o HTLV-1 e a estrongiloidíase.

Strongyloidiasis is one of most important forms of helminthiasis in tropical countries and epidemiologic studies have shown the association of this parasitic disease with HTLV. It has been observed in regions where both these agents are endemic and coinfection may result in an increase in the disseminated forms of strongyloidiasis as well as recurrent strongyloidiasis. While HTLV-1 is related to a high production of IFN-gamma; and deviation of the immune response towards a Th1 response, the protection against helminths is associated with Th2 like immune response. Individuals infected with HTLV and S. stercoralis have a reduction in the production of IL-4, IL-5, IL-13 and parasitic IgE response, all of which are factors participating in the defense mechanism against S. stercoralis. These abnormalities are the basis for the occurrence of an increase in the severe forms of strongyloidiasis among patients infected with HTLV-1.