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HTLV-1 Infection (htlv-1 + infection)
Selected AbstractsHPRT mutations, TCR gene rearrangements, and HTLV-1 integration sites define in vivo T-cell clonal lineages,ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 2-3 2005Mark Allegretta Abstract HPRT mutations in vivo in human T-lymphocytes are useful probes for mechanistic investigations. Molecular analyses of isolated mutants reveal their underlying mutational changes as well as the T-cell receptor (TCR) gene rearrangements present in the cells in question. The latter provide temporal reference points for other perturbations in the in vivo clones as well as evidence of clonal relationships among mutant isolates. Immunological studies and investigations of genomic instability have benefited from such analyses. A method is presented describing a T-cell lineage analysis in a patient with HTLV-1 infection. Lineage reconstruction of an in vivo proliferating HPRT mutant clone allows timing of the integration event to a postthymic differentiated cell prior to the occurrence of HPRT mutations. Environ. Mol. Mutagen., 2005. © 2005 Wiley-Liss, Inc. [source] HTLV-1 infection in blood donors from the Western Brazilian Amazon region: Seroprevalence and molecular study of viral isolatesJOURNAL OF MEDICAL VIROLOGY, Issue 11 2008Aline Cristina Mota-Miranda Abstract To determine the seroprevalence of HTLV-1 in Brazil, and to review the virus molecular epidemiology in this Amazon population (Rio Branco-Acre), 219 blood donors were screened for HTLV-1. Only one case of infection (0.46% seroprevalence) was detected during July 2004 screening at the Acre Hospital Foundation (FUNDACRE). Neighbor-joining and Maximum Likelihood phylogenetic analyses of two (n,=,2) complete LTR region sequences were performed with the PAUP* software. Since the HTLV-1 envelope surface (gp46) and transmembrane (gp21) glycoproteins are important for virus fitness, three envelope glycoproteins sequences (n,=,3) were analyzed using the Prosite tool to determinate potential protein sites. Phylogenetic analysis demonstrated that the new isolate described in this study, and the unpublished LTR strain described in a previous report belong to the Transcontinental subgroup of the Cosmopolitan subtype, inside the Latin American cluster. A similar result was obtained when submitting, to the Automated Genotyping System, three LTR partial sequences from a previous study of the seroprevalence of HTLV-1 in the same Amazon population. In all analyzed env sequences, the potential protein site was found: two PKC phosphorylation sites at amino acid (aa) positions 310,312 and 342,344, one CK2 phosphorylation site at 194,197aa, three N -glycosylation sites at 222,225aa, 244,247aa and 272,275aa, and a single N -myristylation site at 327,338aa. In conclusion, potential protein sites described in HTLV-1 gp46 and gp21 confirm the presence of conserved sites in the HTLV-1 envelope proteins, likewise phylogenetic analysis suggests a possible recent introduction of the virus into North Brazil. J. Med. Virol. 80:1966,1971, 2008. © 2008 Wiley-Liss, Inc. [source] Phylogenetic and molecular analysis of HTLV-1 isolates from a medium sized town in Northern of Brazil: Tracing a common origin of the virus from the most endemic city in the country,JOURNAL OF MEDICAL VIROLOGY, Issue 11 2008Themístocles Magalhães Abstract Salvador-Bahia has the highest prevalence of HTLV-1 infection in Brazil; about 2% of the population is infected. In this city, the prevalence of HTLV in pregnant women is 1%. There is no data of the HTLV-1 prevalence in others cities of the Bahia's Recôncavo, where the population has similar social and demography characteristics to those from Salvador. Our aim was to evaluate the seroprevalence of HTLV in pregnant women in Cruz das Almas-Bahia, a medium-sized city from the Bahia's Recôncavo. All individuals were tested for HTLV (ELISA) and the positive samples were confirmed by Western Blot. Phylogenetic analyses of the total LTR region were performed in all positive samples. We tested 408 samples (45.4% of the estimate pregnant women population) between June 1st and October 31, 2005. The prevalence of HTLV-1 infection was 0.98%. In addition, all isolated virus were grouped in the subtype HTLV-1a, in the Latin American group. Our results suggest that the introduction of HTLV-1 occurred after the slave trade into Salvador. In addition, HTLV-1-infection should be screened during the pregnancy in women originating from HTLV-1 endemic areas. J. Med. Virol. 80:2040,2045, 2008. © 2008 Wiley-Liss, Inc. [source] Presence of tropical spastic paraparesis/human T-cell lymphotropic virus type 1-associated myelopathy (TSP/HAM)-like among HIV-1-infected patients,JOURNAL OF MEDICAL VIROLOGY, Issue 3 2008Jorge Casseb Abstract Human immunodeficiency virus type 1 (HIV-1) and human T-cell lymphotropic virus types 1 and 2 (HTLV-1 and -2) are retroviruses that share similar routes of transmission and some individuals may have a dual infection. These co-infected subjects may be at increased risk for tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HAM)-like. To study the prevalence of tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HAM) among co-infected HIV-1/HTLV-1 subjects. Since July 1997, our group has been following a cohort to study the interaction of HTLV with HIV and/or hepatitis C virus (HCV), as well as HTLV-1-only infected asymptomatic carriers or those already presenting with TSP/HAM. During these 9 years, 296 HTLV-1-infected individuals were identified from a total of 538 patients who were referred to our clinic at the Institute of Infectious Diseases "Emílio Ribas," in São Paulo, Brazil. All subjects were evaluated by two neurologists, blinded to the HTLV status. TSP/HAM diagnosis was based on Kagoshima diagnostic criteria. Results: A total of 38 HIV-1/HTLV-1 co-infected subjects were identified in this cohort: Twenty-six had already been diagnosed with AIDS and 12 remained asymptomatic. Six of 38 co-infected subjects (18%) were diagnosed as having TSP/HAM and also AIDS, and for 5 of them TSP/HAM was their first illness. One additional incident case was diagnosed after 2 years of follow-up. No modifications on HIV-1 viral load was seen. In contrast, the co-infected with TSP/HAM-like group showed higher HTLV-1 proviral load (505,±,380 vs. 97,±,149 copies/104 PBMC, P,= 0.012) than asymptomatic co-infected subjects, respectively. The incidence of myelopathy among HIV-1/HTLV-1 co-infected subjects is probably higher than among patients infected only with HTLV-1, and related to a higher HTLV-1 proviral load. Thus, HTLV-1/2 screening should be done for all HIV-1-infected patients in areas where HTLV-1 infection is endemic. J. Med. Virol. 80:392,398, 2008. © 2008 Wiley-Liss, Inc. [source] Adult T-cell leukaemia/lymphoma-like human T-cell leukaemia virus-1 replication in infective dermatitisBRITISH JOURNAL OF HAEMATOLOGY, Issue 3 2003Anne-Sophie Gabet Summary. Adult T-cell leukaemia/lymphoma (ATLL) is a malignant T-cell proliferation that occurs in 3,5% of individuals infected with human T-cell leukaemia virus-1 (HTLV-1). HTLV-1 infection is also linked to the development of infective dermatitis (ID), an exudative dermatitis of children that has been proposed as a cofactor of ATLL. Here, HTLV-1 replication was investigated over time in a girl with ID and multiparasitic infestation including strongyloidiasis, a disease also known to predispose HTLV-1 carriers to ATLL. Quantitative polymerase chain reaction (PCR) revealed extremely high proviral loads. During the 2-year period of the present study, the proportion of circulating infected cells ranged between 12% and 36%. Quadruplicate linker-mediated PCR amplification of HTLV-1 flanking sequences identified a pattern of extensive and persistent oligoclonal expansion of infected lymphocytes. As viral loads, both the number and the degree of infected T-cell expansion were independent of treatment or clinical signs. However, the temporal fluctuation of proviral loads correlated significantly with the degree of infected T-cell expansion, but not with the overall number of detected clones. This pattern of HTLV-1 replication over time is very different from that observed in asymptomatic carriers and reminiscent of that observed in ATLL, a result consistent with the proposal of ID as an ATLL cofactor. [source] | ||||||||||