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Results for “HTLV-I Infections”

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At least 19 recordsLinked to original sources
PubMed1992

Evidence of preferential female prevalence of HTLV-I associated tropical spastic paraparesis in Bahia-Brazil.

In order to evaluate the prevalence of HTLV-I infection and its association with tropical spastic paraparesis (TSP) in Bahia, a Northeastern State of Brazil, CSF and sera from TSP patients and CSF and/or sera from some selected groups of individuals were studied. The results seem to indicate a higher prevalence of HTLV-I infection in women than men with TSP and among individuals of HIV risk groups. Some alterations of routine analysis of CSF can suggest HTLV-I infection in TSP patients.

Adult↗
PubMed1992

Inefficient transmission of HTLV-I to MOLT-4 cells by cell-free virus and cocultivation.

Transmission of human T cell leukemia virus type I (HTLV-I) to a T cell line (MOLT-4#8) was studied using cell-free virus infection or cocultivation with an HTLV-I-transformed T cell line (MT-2). Immunofluorescence and FACS analyses showed that HTLV-I was efficiently adsorbed onto MOLT-4#8 cells. However, after adsorption, no extrachromosomal viral DNA in the cells was detected by the Southern blot method. In contrast, when MT-2 cells were cocultured with MOLT-4#8 cells, generation of extrachromosomal DNA was clearly observed. These data suggest that the cell-free HTLV-I may have difficulties in penetration, uncoating or reverse transcription. After cocultivation, MOLT-4#8 cells chronically infected with HTLV-I were cloned and analyzed. Only four provirus-positive cell lines were obtained. The transmission rate of the virus by cocultivation seemed to be low in our experimental system, although marked cell fusion was observed. Moreover, none of the cloned cell lines which harbored HTLV-I provirus expressed any viral protein. Inefficient integration and expression of the provirus might be hypothesized as compared with human immunodeficiency virus type 1 transmission.

Cell Fusion↗
PubMed1992

Detection of HTLV-I in clinical specimens.

The American Red Cross, which collects 50% of blood for transfusion in the United States, now tests all prospective blood donors for HTLV-I and HTLV-II antibodies. It will therefore be important to recognize the significance and clinical spectrum of diseases associated with these viruses, and to become familiar with the current methods used to diagnose infection. This review summarizes the techniques currently in use to screen for HTLV-I/II antibodies, as well as methods to detect viral genome and/or gene products in blood and tissue specimens.

Deltaretrovirus Antigens↗
PubMed1992

Development of a monoclonal antibody-based p24 capsid antigen detection assay for HTLV-I, HTLV-II, and STLV-I infection.

A monoclonal antibody-based antigen capture enzyme-linked immunosorbent assay (ELISA) was developed and employed to detect p24 capsid antigen from human T-cell lymphotropic viruses type I and II (HTLV-I, HTLV-II), simian T-cell lymphotropic virus type I (STLV-I)-infected cell lines, and from mononuclear cell cocultures of HTLV-infected humans and STLV-I infected monkeys. A monoclonal antibody specific for HTLV p24 and p53 capsid antigens was coated onto 96-well microtiter plates to capture HTLV/STLV antigen. Captured antigen was then detected by the addition of a polyclonal, biotinylated human anti-HTLV-I antibody, and color developed with tetramethyl benzidine/H2O2 substrate. As little as 15 pg/ml of HTLV-I p24 antigen could be detected in this assay. Culture supernatants from HTLV-I-infected cell lines (HUT-102, MT-2, C5/MJ, HTLV-II-infected cell lines (Mo-T, Mo-B, PanG 12.1, NRA) and STLV-I-infected cell lines (Matsu, NEPC M39) were all positive in the assay. In addition, p24 was detected from peripheral blood mononuclear cell (PBMC) cocultures of 8 of 8 (100%) HTLV-I diseased patients, 14 of 20 (70%) HTLV-I and HTLV-II-infected, asymptomatic persons, and 8 of 8 (100%) STLV-I-infected, asymptomatic monkeys. Culture supernatants of cells infected with human immunodeficiency virus type (HIV-1), simian immunodeficiency virus (SIV), Chlamydia trachomatis, cytomegalovirus (CMV), herpes simplex I and II (HSV), feline leukemia virus (FELV), bovine leukemia virus (BLV), and bovine immunodeficiency virus (BIV) were all negative. Similarly, normal human peripheral blood mononuclear cells and uninfected, transformed human T cells, were also negative in the assay.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗
PubMedDate not supplied

[Sarcoidosis and leukemia/T-cell lymphoma associated with HTLV-1 virus infection in adults (apropos of a case)].

The HTLV-1 virus causes a disturbance of the immune system, the evaluation of which is often difficult. We report a case of sarcoidosis in a 49 year old woman of Martinique as evidenced by bilateral hilar adenopathy, hypercalcaemia, uveitis and granulomatous lesions on histological examination. Serological was positive for HTLV-1 antibodies. Three years later she developed an adult T-cell leukemia/lymphoma. The relationships between the HTLV-1 retroviral infection and different pathologies observed are discussed.

Female↗
PubMed1992

Parathyroid hormone-related protein binding to human T-cell lymphotropic virus type I-infected lymphocytes.

An HTLV-I-infected human lymphocyte line (MT-2) was evaluated for 1) the presence of receptors for PTH-related protein (PTHrP), 2) cell proliferation in response to PTHrP, and 3) adrenylate cyclase and intracellular calcium response to PTHrP. PTHrP-(1-36) was labeled with 125I, purified, and used to detect binding to MT-2 cells. Specific binding ranged between 4-9% of the total radioactivity. Specific binding increased with increasing cell number, was maximal within 30-60 min, and was highest at 37 C. Scatchard analysis revealed a one-binding site fit, with a Kd of 14.5 nM. Binding was not competed for by calcitonin, calcitonin gene-related peptide, or interleukin-1 beta. PTHrP at 1.0 and 0.1 microM inhibited proliferation in MT-2 cells. PTHrP did not alter adenylate cyclase stimulation in MT-2 cells, but did cause an increase in intracellular calcium. These findings indicate that MT-2 cells have receptors for PTHrP and are consistent with a potential autocrine role of PTHrP in HTLV-I-infected lymphoid cells.

Adenylyl Cyclases↗
PubMed2025

High expression of Rex-orf-I and HBZ mRNAs and bronchiectasis in lung of HTLV-1A/C infected macaques.

HTLV-1 type-A rarely causes lung disease in humans, whereas HTLV-1 type-C is more frequently associated with respiratory failure and premature death. We investigated the genetic basis of HTLV-1C morbidity by constructing a chimeric HTLV-1A/CoI-L encompassing the highly divergent type C orf-I. We demonstrate that systemic infectivity of HTLV-1A and HTLV-1A/CoI-L is equivalent in macaques, but viral expression in lungs is significantly higher in HTLV-1A/CoI-L infection. In addition, bronchoalveolar-lavage immune cell dynamics differs greatly with neutrophils and monocytes producing TNF-α in HTLV-1A/CoI-L, but producing IL-10 in HTLV-1A infection. Animals infected with HTLV-1A/CoI-L develops bronchiectasis at 10 months from infection, but at the same timepoint those infected with HTLV-1A do not. HTLV-1A/CoI-L expressed a 16 kDa fusion protein (p16C) via a doubly spliced, Rex-orf-IC, mRNA able to shield T-cells from efferocytosis, a monocyte function that mitigates inflammation via clearance of apoptotic cells. The Rex-orf-IC mRNA is expressed as more frequent in the lung of HTLV-1A/CoI-L than HTLV-1A infected animals. Since defective efferocytosis is associated with lung obstructive pathologies, the data raise the hypothesis that p16C may contribute to the lung morbidity observed in HTLV-1C infection.

Animals↗
PubMed1992

Imaging of human T-lymphotropic virus type I-associated chronic progressive myeloneuropathies.

We studied magnetic resonance imaging (MRI) of the head and cervical spine and CT of the head in 46 patients (14 men, 32 women) with chronic progressive myeloneuropathy. The findings were correlated with human T-lymphotropic virus type I (HTLV-I) serology, race, country of origin, and age. We found a female predominance of 2:1. Most patients were aged between 30 and 50 years, and most were Caribbean immigrants and black. There were 9 men and 17 women with blood antibody titers to HTLV-I and 7 men and 15 women with cerebrospinal fluid (CSF) titers. All patients with virus or antibodies in blood or CSF were Caribbean immigrants or black. T2-weighted cranial MRI showed scattered areas of high signal intensity in the cerebral white matter, usually in the periventricular and subcortical areas, but not in the posterior cranial fossa. Cranial CT revealed periventricular low density areas, ventricular enlargement, and atrophy MRI of the cervical spine showed atrophy of the cord. Myelography was normal in all 15 patients examined. No imaging differences were observed between the HTLV-I-positive and -negative patients. These findings, although consistent with demyelination, are not specific.

Adolescent↗
PubMed2025

A viral clonality evenness score to predict progression to adult T-cell leukaemia in asymptomatic carriers of human T-lymphotropic virus type 1 in Japan: a retrospective longitudinal cohort study.

BACKGROUND: Adult T-cell leukaemia/lymphoma (ATL) is a highly aggressive T-cell malignancy that occurs in approximately 2-7% of individuals with human T-lymphotropic virus type 1 (HTLV-1), after decades of asymptomatic infection. To address the urgent need for predictive biomarkers to identify asymptomatic carriers of HTLV-1 at high risk of progression to ATL, we aimed to evaluate viral clonality sequencing as a potential tool for risk stratification. METHODS: This retrospective longitudinal cohort study involved HTLV-1 carriers enrolled in the Joint Study on Predisposing Factors of ATL Development, a nationwide cohort study initiated in Japan in 2002. Participants were selected from this cohort on the basis of their baseline proviral load at the time of enrolment as an asymptomatic carrier, length of follow-up, and clinical outcome. The cohort was subdivided into three subgroups: the first comprising HTLV-1 carriers who developed ATL, the second comprising carriers with high proviral load (&#x2265;4%) who did not progress to ATL, and the third comprising carriers with low proviral load (<4%) who did not progress to ATL. DNA extracted from peripheral blood mononuclear cells collected at enrolment and at least one follow-up visit was analysed by HTLV-1 clonality sequencing and the proviral load was quantified. We calculated a viral clonality evenness (VCE) score, based on the Shannon Evenness Index, to quantify the uniformity of the clonal distribution of samples, for which 0 represents a perfectly monoclonal architecture and 1 indicates a completely polyclonal landscape. We then estimated the performance of proviral load thresholds and VCE scoring to classify the risk of progression to ATL using the area under the receiver operating characteristic curve (AUC), the accuracy, and Matthews correlation coefficient. VCEs were compared between participant subgroups with the Wilcoxon rank sum test. FINDINGS: 56 participants followed up by JSPFAD between Feb 6, 2003, and July 19, 2022, were included in this study: 17 who progressed to ATL (mean follow-up 8&#xb7;3 years [SD 4&#xb7;0]), 18 who had a high proviral load and did not progress to ATL (9&#xb7;7 years [3&#xb7;4]), and 21 who had a low proviral load and did not progress to ATL (7&#xb7;5 years [3&#xb7;0]). Clonality sequencing of samples from 39 participants who did not progress to ATL revealed hundreds to thousands of HTLV-1 integration sites at both timepoints, corresponding to multiple clones of low and uniform abundance, and these participants had high VCE scores (&#x2265;0&#xb7;694) at baseline. By contrast, most participants (14 of 17) who progressed to ATL had a single predominant clone or two to four predominant clones at both timepoints, and lower VCE scores (<0&#xb7;694) at baseline than those who did not progress (p<0&#xb7;0001). AUCs were very similar for proviral load thresholds (91 [95% CI 80-98]) and VCE scoring (91 [78-100]), although when using methods that give equal weight to every individual, VCE scoring outperformed proviral load thresholds in predicting progression to ATL (accuracy: proviral load 0&#xb7;76 [95% CI 0&#xb7;76-0&#xb7;77], VCE scoring 1&#xb7;00 [0&#xb7;99-1&#xb7;00]; Matthews correlation coefficient: proviral load 0&#xb7;23 [95% CI 0&#xb7;19-0&#xb7;24], VCE scoring 0&#xb7;91 [0&#xb7;80-1&#xb7;00]). Prediction based on VCE scoring indicated no false positives, compared with 20% when using proviral load, although VCE scoring yields a greater number of false negatives (0&#xb7;3% vs 0&#xb7;1%). INTERPRETATION: The implementation of VCE scoring in clinical practice could inform early pre-emptive therapeutic interventions, exclusively targeting individuals with HTLV-1 at high risk and aiming to prevent progression to aggressive, treatment-refractory disease. Further validation, including independent confirmation of the performance of VCE scoring in multiple populations and the characterisation of its temporal dynamics, will be crucial to determine its clinical utility and potential integration into care pathways. FUNDING: Association Jules Bordet, FNRS-T&#xe9;l&#xe9;vie, FCC, WALInnov, FLF, JSPS-KAKENHI, and CoBiA.

Humans↗
PubMed2025

Role of the CTCF binding site in Human T-Cell Leukemia Virus-1 pathogenesis.

During HTLV-1 infection, the virus integrates into the host cell genome as a provirus with a single CCCTC binding protein (CTCF) binding site (vCTCF-BS), which acts as an insulator between transcriptionally active and inactive regions. Previous studies have shown that the vCTCF-BS is important for maintenance of chromatin structure, regulation of viral expression, and DNA and histone methylation. Here, we show that the vCTCF-BS also regulates viral infection and pathogenesis in vivo in a humanized (Hu) mouse model of adult T-cell leukemia/lymphoma. Three cell lines were used to initiate infection of the Hu-mice, i) HTLV-1-WT which carries an intact HTLV-1 provirus genome, ii) HTLV-1-CTCF, which contains a provirus with a mutated vCTCF-BS which abolishes CTCF binding, and a stop codon immediately upstream of the mutated vCTCF-BS which deletes the last 23 amino acids of the p12 gene, and iii) HTLV-1-p12stop that contains the intact vCTCF-BS, but retains the same stop codon in p12 as in the HTLV-1-CTCF cell line. Hu-mice were infected with mitomycin-treated or irradiated HTLV-1 producing cell lines. There was a delay in pathogenicity when Hu-mice were infected with the HTLV-1-CTCF virus compared to mice infected with either HTLV-1-p12 stop or HTLV-1-WT virus. Proviral load (PVL), spleen weights, and CD4 T cell counts were significantly lower in HTLV-1-CTCF infected mice compared to HTLV-1-p12stop infected mice. Furthermore, we found a direct correlation between the PVL in peripheral blood and death of HTLV-1-CTCF infected mice. In cell lines, we found that the vCTCF-BS regulates Tax expression in a time-dependent manner. The scRNAseq analysis of splenocytes from infected mice suggests that the vCTCF-BS plays an important role in activation and expansion of T lymphocytes in vivo. Overall, these findings indicate that the vCTCF-BS regulates Tax expression, proviral load, and HTLV pathogenicity in vivo.

Human T-lymphotropic virus 1↗
PubMed1992

[Three cases of chronic respiratory tract lesions associated with adult T-cell leukemia (ATL)].

Three cases of chronic respiratory tract lesions as a complication of adult T-cell leukemia (ATL) are reported. Case 1 was seropositive for HTLV-1 on recent examination following treatment of bronchiolitis. Chest radiograph revealed over inflation of the lungs and bilateral diffuse small nodular shadows. Pulmonary function test resulted hypoxemia and mixed ventilation disorder. Pathological examination confirmed lymphocytic infiltration of the bronchiolar wall. Both clinically and pathologically the patient was diagnosed as having diffuse panbronchiolitis (DPB). Therefore, this case was considered to be the bronchiolar type of HTLV-1 associated bronchiolo-alveolar disorder (HABA). The other two cases with smoldering or chronic ATL presented with long-standing symptoms of productive cough due to chronic respiratory lesions. We consider that all three cases had HTLV-1 virus associated pulmonary lesions, but with different clinical and pathological presentations. Among 12 cases of bronchiolitis experienced at our hospital, three were positive for HTLV-1.

Adult↗
PubMed1992

Detection of simian T-lymphotropic virus type I using the polymerase chain reaction.

To develop the polymerase chain reaction (PCR) for the detection of simian T-lymphotropic virus type I (STLV-I) infection, cell lines or peripheral-blood mononuclear cells (PBMC) from 2 non-human primate species [African green monkeys (AGM), Cercopithecus aethiops; baboon, Papio cynocephalus] were evaluated for their STLV-I status using oligonucleotide primer pairs and probes specific for the tax and pol gene regions of the closely related human T-lymphotropic virus type I (HTLV-I). These PCR results were compared with serologic (Western blot assay) and viral culture (p24-antigen capture assay) data. PCR products for both gene regions were detected in established baboon, Japanese macaque and rhesus macaque STLV-I-producing cell lines. STLV-I tax and pol products were also detected in PBMC from 4 of 4 infected AGM and 4 of 4 infected baboons, each of which were also Western-blot-positive and p24-antigen-capture-positive. Of the remaining AGM (n = 7) and baboon (n = 1) which were PCR-negative, each was also Western-blot-negative and p24-antigen-capture-negative. Two seronegative and virus-culture-negative AGM were classified as PCR indeterminate with weak reactivity using tax primers. These primer pairs failed to amplify DNA from uninfected human PBMC, an uninfected human lymphoid cell line, a simian immunodeficiency virus macaque (SIVmac251)-infected cell line and a simian-retrovirus-type-D(SRV-D)-infected cell line. HTLV-II-pol-specific primer pairs failed to amplify DNA from STLV-I-infected cell lines and PBMC from STLV-I-infected monkeys. Further, HTLV-I pol and tax primer pairs successfully amplified RNA from HTLV-I- and STLV-I-infected cell lines by reverse transcriptase (RT)-PCR. We have demonstrated excellent specificity in the detection of STLV-I by PCR using these HTLV-I-derived primers and probes. Additionally, our data suggest that the tax and pol gene regions are conserved between HTLV-I and STLV-I strains found among these diverse species of non-human primates.

Animals↗
PubMedDate not supplied

Primary B cell lymphoma of the rectum in a patient coinfected with HIV-1 and HTLV-I.

This report describes a clinical case of a large cell, immunoblastic plasmacytoid malignant B-cell lymphoma of the rectum in an AIDS patient coinfected with HTLV-I. The malignant cells showed clonal genetic rearrangement of the HC (JH) and LCK genes. Infection by EBV was demonstrated serologically and with slot blots using genomic DNA of the cancer cells. Southern blot analysis with DNA extracted from the lymphoma cells were negative for HTLV-I. The patient received seven cycles of VACO-B which induced complete but transient clinical remission of the tumor. The final outcome of the patient is unknown.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Monitoring for HIV-1, HIV-2, HTLV-I sero-progression and sero-conversion in a population at risk in east Africa.

Thirty-three individuals from East Africa, at risk for acquiring sexually transmitted infections, were selected to be monitored over a five month period for evidence of sero-progression and/or sero-conversion for human immunodeficiency virus type-1 and type-2 (HIV-1, HIV-2), and human T cell leukemia virus type-1 (HTLV-I). Initially, all sera were reactive by at least one retroviral screening assay, but most produced negative or indeterminate results by western blot assays. Five months after the initial screening, western blot assays indicated that one individual exhibited full sero-conversion for HIV-1; one HIV-1 positive individual also became positive for HIV-2; and two subjects showed sero-progression to become HTLV-I confirmed positive. Sera from fourteen individuals produced indeterminate results by western blot for HIV-1, ten of which were previously negative; the remaining four sera exhibited reactivity to at least one additional viral specific antigen after the five months. Circulating HIV-1 antigen was not demonstrated in any of the sera but DNA isolated from one of the individuals with indeterminate results produced a positive reaction for HIV-1 by the polymerase chain reaction.

Blotting, Western↗