OBJECtIVE: this study aimed to describe a syndrome thatthe authors call human t-lymphotropic virus type I-related chronic interstitial keratitis. MEtHODS: A consecutive series of 194 human t-lymphotropic virus type I...
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OBJECtIVE: this study aimed to describe a syndrome thatthe authors call human t-lymphotropic virus type I-related chronic interstitial keratitis. MEtHODS: A consecutive series of 194 human t-lymphotropic virus type I-infected patients (divided into 119 patients with human t-lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis and 75 asymptomatic human t-lymphotropic virus type I carriers) was systematically examined. RESULtS: twenty patients (10.3%) had bilateral anterior stromal lesions made up of approximately 10 elevated, rounded or cloudy whitish opacities that were more or less confluent. the opacities were characteristically situated atthe periphery of the anterior stroma, and the visual axis remained unaffected, the interstitial keratitis was chronic and unresponsive to topical administration of corticosteroids. It was mainly observed in patients affected by human t-lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis among whom there were 18 cases (15.1%), as opposed to two cases (2.7%) in asymptomatic carriers. CONCLUSION: A new cause of interstitial keratitis is reported. Human t-lymphotropic virus type I infection may have a much broader spectrum of ocular manifestations than previously described. As with the other manifestations of human t-lymphotropic virus type I infection, corneal lesions could be linked to a lymphoplasmocytic infiltration of the stroma leading to corneal opacities. (Am J Ophthalmol 2001;131:305-308. (C) 2001 by Elsevier Science Inc, All rights reserved.).
PURPOSE: to examine the cause of adultt-cell leukemia/ lymphoma. MEtHODS: We examined a conjunctival biopsy from a 29-year-old Jamaican man who developed bilateral conjunctival masses. Adultt-cell leukemia/lymphoma ...
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PURPOSE: to examine the cause of adultt-cell leukemia/ lymphoma. MEtHODS: We examined a conjunctival biopsy from a 29-year-old Jamaican man who developed bilateral conjunctival masses. Adultt-cell leukemia/lymphoma was diagnosed using routine histology, immunohistochemistry, electron microscopy, microdissection, and the polymerase chain reaction. RESULtS: Histopathologic examination revealed a conjunctival lymphoma. Clonality of the t-cell receptor gamma gene and human t-cell lymphotrophic virus gag gene were detected in the malignant cells. the demonstration of the human t-cell lymphotrophic virus gene and the rearrangement of the t-cell receptor gene in this neoplasm provide proof that human t-cell lymphotrophic virus is the cause of this conjunctival t-cell lymphoma, CONCLUSION: Human t-cell lymphotrophic virus is the cause of adultt-cell leukemia/lymphoma, an aggressive malignancy of CD4+ lymphocytes. (Am J Ophthalmol 2001;131:381-383, (C) 2001 by Elsevier Science Inc. All rights reserved.).
PURPOSE: Human t-cell lymphotrophic virus type 1 is a RNA retrovirus that primarily affects CD4+ t-cells. Human t-cell lymphotrophic virus type 1 infection is the established cause of adultt-cell leukemia/lymphoma, a...
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PURPOSE: Human t-cell lymphotrophic virus type 1 is a RNA retrovirus that primarily affects CD4+ t-cells. Human t-cell lymphotrophic virus type 1 infection is the established cause of adultt-cell leukemia/lymphoma, an aggressive malignancy of CD4+ t-cells, and two non-neoplastic conditions: human t-cell lymphotrophic virus type 1-associated myelopathy/tropical spastic paraparesis and human t-cell lymphotrophic virus type 1 uveitis. Other reported ophthalmic manifestations of human t-cell lymphotrophic virus type I infection include lymphomatous and leukemic infiltrates in the eye and ocular adnexa in patients with adultt-cell leukemia/lymphoma, retinal pigmentary degeneration, and neuro-ophthalmic disorders in patients with human t-cell lymphotrophic virus type 1-associated myelopathy/tropical spastic paraparesis and keratoconjunctivitis sicca, episcleritis, and sclerouveitis in asymptomatic human t-cell lymphotrophic virus type I carriers. this report describes the ocular findings in three Jamaican patients with human t-cell lymphotrophic virus type 1 infection and adultt-cell leukemia/lymphoma. MEtHODS: the clinical records of three patients with human t-cell lymphotrophic virus type 1 infection and adultt-cell leukemia/lymphoma examined atthe National Eye Institute were reviewed. Each patient had one or more complete ophthalmic evaluations. RESULtS: All three patients had corneal abnormalities, including corneal haze and central opacities with thinning;bilateral immunoprotein keratopathy;and peripheral corneal thinning, scarring, and neovascularization. All three patients had elevated serum immunoglobulin levels. CONCLUSIONS: We believe thatthe novel corneal findings in these patients are most likely a consequence of the hypergammaglobulinemia induced by the human t-cell lymphotrophic virus type 1 infection or the t-cell malignancy. (Am J Ophthalmol 2001;131:309-313. (C) 2001 by Elsevier Science Inc. All rights reserved.).
the risk of disease associated with persistent virus infections such as HIV-I, hepatitis B and C, and human t-lymphotropic virus-I (HtLV-I) is strongly determined by the virus load. However, it is not known whether a ...
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the risk of disease associated with persistent virus infections such as HIV-I, hepatitis B and C, and human t-lymphotropic virus-I (HtLV-I) is strongly determined by the virus load. However, it is not known whether a persistent class I HLA-restricted antiviral cytotoxic t lymphocyte (CtL) response reduces viral load and is therefore beneficial or causes tissue damage and contributes to disease pathogenesis. HtLV-I-associated myelopathy (HAM/tSP) patients have a high virus load compared with asymptomatic HtLV-I carriers, We hypothesized that HLA alleles control HtLV-I provirus load and thus influence susceptibility to HAM/tSP. Here we show that, after infection with HtLV-I, the class I allele HLA-A*02 halves the odds of HAM/tSP (P < 0.0001), preventing 28% of potential cases of HAM/tSP. Furthermore, HLA-A*02(+) healthy HtLV-I carriers have a proviral load one-third that (P = 0.014) of HLA-A*02(-) HtLV-I carriers, An association of HLA-DRB1*0101 with disease susceptibility also was identified, which doubled the odds of HAM/tSP in the absence of the protective effect of HLA-A*02. these data have implications for other persistent virus infections in which virus load is associated with prognosis and imply that an efficient antiviral CtL response ran reduce virus load and so prevent disease in persistent virus infections.
the Mt-2 cell line transformed by human t-cell leukemia virus type 1 (HtLV-1) contains one complete provirus and seven defective proviruses. Four defective genomes have an identical structure (LtR-MA-delta CA-pX-LtR) ...
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the Mt-2 cell line transformed by human t-cell leukemia virus type 1 (HtLV-1) contains one complete provirus and seven defective proviruses. Four defective genomes have an identical structure (LtR-MA-delta CA-pX-LtR) with an open reading frame that spans from MA to pX, giving rise to a 3.4-kb (24S) RNA transcript encoding a chimeric Gag-pX protein, p28. Mt-2 cells release two distincttypes of virions. the major "classic" type of particle has a buoyant density of 1.155-1.16 g/cm(3) and contains the standard HtLV-I structural proteins and reverse transcriptase (Rt). In addition, about 5% of particles are "light" approximately 1.12 g/cm(3), and contain p28, Rt activity, and the 3.4-kb RNA transcript. Rt-PCR and in vitro translation indicate that some of the classic HtLV-I particles package 3.4-kb RNA as well as full-length 8.5-kb RNA. In addition to matrix features, the p28 protein has a motif resembling a zinc finger atthe C-terminal, pX0 region, which may play a role in the assembly of the defective light virions. (C) 1999 Academic Press.
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