pmid title sentence year journal region virus mutation mutation_start mutation_end gene gene_start gene_end disease disease_start disease_end 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. 2018 Virology journal Title HTLV1 N93D 141 145 gp46;gp46 24;41 39;45 34343702 The N93D mutation of the human T-cell leukemia virus type 1 envelope glycoprotein found in symptomatic patients enhances neuropilin-1 b1 domain binding. The N93D mutation of the human T-cell leukemia virus type 1 envelope glycoprotein found in symptomatic patients enhances neuropilin-1 b1 domain binding. 2021 Biochimica et biophysica acta. Proteins and proteomics Title HTLV1 N93D 4 8 Env 60 68 10343169 Analysis of potential phosphorylation sites in human T cell leukemia virus type 1 Tax. Analysis of selected Tax mutants for ability to trans-activate the cytomegalovirus promoter demonstrated mutation of serine 77 to alanine reduced trans-activation by 90% compared to wild-type Tax. 1999 Journal of biomedical science Abstract HTLV1 S77A 117 137 Tax;Tax 21;192 24;195 10435578 Four A6-TCR/peptide/HLA-A2 structures that generate very different T cell signals are nearly identical. The three-dimensional structures of the three A6-TCR/peptide/HLA-A2 complexes are remarkably similar to each other and to the wild-type agonist complex, with minor adjustments at the interface to accommodate the peptide substitutions (P6A, V7R, and Y8A). 1999 Immunity Abstract HTLV1 P6A;Y8A;V7R 235;249;240 238;252;243 10516045 Amino acid changes at positions 173 and 187 in the human T-cell leukemia virus type 1 surface glycoprotein induce specific neutralizing antibodies. We thus identified two amino acid changes, I173-->V and A187-->T, that play an important role in the antigenicity of neutralizable epitopes located in this region of the surface envelope glycoprotein. 1999 Journal of virology Abstract HTLV1 I173V;A187T 43;56 51;64 Env 178 186 10567539 PCAF interacts with tax and stimulates tax transactivation in a histone acetyltransferase-independent manner. Point mutations at Tax amino acid 318 (TaxS318A) or 319 to 320 (Tax M47), which have decreased or no activity on the HTLV-1 promoter, are defective for PCAF binding. 1999 Molecular and cellular biology Abstract HTLV1 S318A;L319R;L320S 42;68;68 47;71;71 Tax;Tax;Tax 19;39;64 22;42;67 10698501 Functional impairment of p73 and p51, the p53-related proteins, by the human T-cell leukemia virus type 1 Tax oncoprotein. Moreover, a mutant Tax of coactivator CBP-binding site (K88A), which activated NF-kappaB but not CREB pathway, could not repress the p73 nor p51 trans-activation functions, indicating that CBP-binding domain of Tax is essential for the suppression of their functions. 2000 Oncogene Abstract HTLV1 K88A 56 60 Tax;Tax 19;211 22;214 10734308 HTLV-1 tax oncoprotein represses the p53-mediated trans-activation function through coactivator CBP sequestration. However, Tax with a mutation in the coactivator CBP-binding site (K88A), which activates NF-kappaB but not the CREB pathway, could not repress the p53 trans-activation function. 2000 Oncogene Abstract HTLV1 K88A 66 70 Tax 9 12 10766811 p300 and p300/cAMP-responsive element-binding protein associated factor interact with human T-cell lymphotropic virus type-1 Tax in a multi-histone acetyltransferase/activator-enhancer complex. The M47 mutant (L319R, L320S) protein, which has previously been shown to interact with p300/CBP, by contrast, failed to form complexes with P/CAF and is impaired in LTR trans-activation. 2000 The Journal of biological chemistry Abstract HTLV1 L319R;L320S 16;23 21;28 LTR 166 169 10766811 p300 and p300/cAMP-responsive element-binding protein associated factor interact with human T-cell lymphotropic virus type-1 Tax in a multi-histone acetyltransferase/activator-enhancer complex. The Tax mutants (K88A and V89A) defective for p300/CBP-binding and LTR trans-activation, retained their abilities to interact with P/CAF. 2000 The Journal of biological chemistry Abstract HTLV1 K88A;V89A 17;26 21;30 LTR;Tax 67;4 70;7 11000222 In vivo analysis of human T-cell leukemia virus type 1 reverse transcription accuracy. Mutation of the methionine residue in the conserved YMDD motif of the HTLV-1 reverse transcriptase to either alanine or valine (i.e., M188A or M188V) led to a factor of two increase in the rate of mutation, indicating the role of this motif in enzyme accuracy. 2000 Journal of virology Abstract HTLV1 M188A;M188V 134;143 139;148 11027594 Antigenicity of chimeric synthetic peptides based on HTLV-1 antigens and the impact of epitope orientation. The peptide M1 is a p19 (105-124) sequence, the peptide M2 is a gp46 (190-207) sequence, and the peptide M3 is a gp 46 sequence with substitution of proline at position 192 by serine. 2000 Biochemical and biophysical research communications Abstract HTLV1 P192S 149 182 gp46 64 68 11046153 Distinct p300-responsive mechanisms promote caspase-dependent apoptosis by human T-cell lymphotropic virus type 1 Tax protein. Importantly, nuclear expression of the minimal CBP/p300-binding peptide of Tax induced apoptosis in the absence of Tax-dependent transcriptional activities, while its K88A counterpart did not cause cell death. 2000 Molecular and cellular biology Abstract HTLV1 K88A 167 171 Tax;Tax 75;115 78;118 11046153 Distinct p300-responsive mechanisms promote caspase-dependent apoptosis by human T-cell lymphotropic virus type 1 Tax protein. The CBP/p300-binding defective Tax mutants K88A and V89A exhibited markedly reduced cytotoxic effects compared to the wild-type Tax protein. 2000 Molecular and cellular biology Abstract HTLV1 K88A;V89A 43;52 47;56 Tax;Tax 31;128 34;131 11070166 Conversion of a T cell antagonist into an agonist by repairing a defect in the TCR/peptide/MHC interface: implications for TCR signaling. Here, we demonstrate that antagonist activity of P6A is associated with low affinity of the A6 alphabetaTCR for Tax-P6A/HLA-A2. 2000 Immunity Abstract HTLV1 P6A;P6A 49;116 52;119 Tax 112 115 11070166 Conversion of a T cell antagonist into an agonist by repairing a defect in the TCR/peptide/MHC interface: implications for TCR signaling. The structure of the A6 alphabetaTCR/HTLV-1 Tax-peptide/MHC I complex with proline 6 of Tax substituted with alanine (P6A), an antagonist, is nearly identical to the structure with wild-type Tax agonist. 2000 Immunity Abstract HTLV1 P6A 118 121 Tax;Tax;Tax 44;88;191 47;91;194 11080799 Kinase-inducible domain-like region of HTLV type 1 tax is important for NF-kappaB activation. Here we report that single (K88A, V89A, L90A) and double alanine substitutions (V89A-L90A) in the (88)KVL(90) motif attenuate the ability of Tax to activate NF-kappaB. 2000 AIDS research and human retroviruses Abstract HTLV1 K88A;V89A;L90A;V89A;L90A 28;34;40;80;85 32;38;44;84;89 Tax 141 144 11080799 Kinase-inducible domain-like region of HTLV type 1 tax is important for NF-kappaB activation. In contrast, although the L90A mutant is similarly attenuated for NF-kappaB activation, it showed significant activity in LTR trans-activation. 2000 AIDS research and human retroviruses Abstract HTLV1 L90A 26 30 LTR 122 125 11080799 Kinase-inducible domain-like region of HTLV type 1 tax is important for NF-kappaB activation. Incorporation of both V89A and L90A substitutions in a V89A-L90A double mutant further reduced NF-kappaB activation and completely abrogated LTR trans-activation. 2000 AIDS research and human retroviruses Abstract HTLV1 V89A;L90A;V89A;L90A 22;31;55;60 26;35;59;64 LTR 141 144 11080799 Kinase-inducible domain-like region of HTLV type 1 tax is important for NF-kappaB activation. The alanine substitutions affect HTLV-1 LTR activation and NF-kappaB activation differently, with K88A and V89A mutants showing much reduced activities for HTLV LTR activation while retaining attenuated but significant NF-kappaB-activating function. 2000 AIDS research and human retroviruses Abstract HTLV1 K88A;V89A 98;107 102;111 LTR;LTR 40;161 43;164 12711052 Naturally occurring substitutions of the human T-cell leukemia virus type 1 3' LTR influence strand-transfer reaction. By contrast, a single G-->A transition at position 52 was found to result in 33% gain of function. 2003 Journal of virological methods Abstract HTLV1 G52A 22 53 12711052 Naturally occurring substitutions of the human T-cell leukemia virus type 1 3' LTR influence strand-transfer reaction. Furthermore, a C-->T transition at 41 bp from the provirus 3' end decreased the reaction efficiency by 80%. 2003 Journal of virological methods Abstract HTLV1 C41T 15 40 14580193 KIX-mediated assembly of the CBP-CREB-HTLV-1 tax coactivator-activator complex. The interaction is disrupted by a single amino acid variation of Tax(59-98) in which leucine 68 is substituted with proline. 2003 Biochemistry Abstract HTLV1 L68P 85 123 Tax 65 68 14645559 The central region of human T-cell leukemia virus type 1 Tax protein contains distinct domains involved in subunit dimerization. Moreover, the Tax mutants M22 (T130A and L131S) and M29 (K189A and R190S), with amino acid substitutions located in DD1 and DD2, respectively, were found to be impaired in Tax self-association. 2003 Journal of virology Abstract HTLV1 T130A;L131S;K189A;R190S 31;41;57;67 36;46;62;72 Tax;Tax 14;172 17;175 16046523 In vivo analysis of replication and immunogenicity of proviral clones of human T-lymphotropic virus type 1 with selective envelope surface-unit mutations. In vitro assays indicate that HTLV-1 envelope (Env) Ser75Ile, Asn95Asp, and Asn195Asp surface unit (SU) mutants are able to replicate in and immortalize lymphocytes. 2005 Blood Abstract HTLV1 S75I;N95D;N195D 52;62;76 60;70;85 Env;Env 37;47 45;50 17050604 Human T-cell leukemia virus type 1 Tax protein down-regulates pre-T-cell receptor alpha gene transcription in human immature thymocytes. Such a decrease is not observed in MOLT-4 cells transduced by a vector encoding the Tax mutant K88A, which is unable to interact with p300. 2007 Journal of virology Abstract HTLV1 K88A 95 99 Tax 84 87 17067264 Distribution of human T cell lymphotropic virus type 1 (HTLV-1) subtypes in Brazil: genetic characterization of LTR and tax region. Five specific nucleotide substitutions, C7401T, T7914C, C7920T, C7982T, and G8231A, were highly conserved among the Brazilian isolates (79.6%), with a frequency ranging from 81.6% to 100% in the sample group and from 18.4% to 24.1% in the prototypes used, suggesting the existence of a molecular signature. 2006 AIDS research and human retroviruses Abstract HTLV1 C7401T;T7914C;C7920T;C7982T;G8231A 40;48;56;64;76 46;54;62;70;82 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Like wild-type tax, many of them (C23W, A108T, L159F, and L235F) transactivate both the HTLV-LTR and the NF-kappaB reporters. 2007 Retrovirology Abstract HTLV1 A108T;L159F;L235F;C23W 40;47;58;34 45;52;63;38 LTR;Tax 93;15 96;18 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. One of them, V19M, preferentially activates NF-kappaB, but is attenuated for LTR activation. 2007 Retrovirology Abstract HTLV1 V19M 13 17 LTR 77 80 17577584 An N-terminal glycine-rich sequence contributes to retrovirus trimer of hairpins stability. Here we show that the reduced fusion activity of an I334A mutant correlated with a decrease in stability of the gp21 trimer of hairpins conformation, in the context of a maltose-binding protein-gp21 chimera. 2007 Biochemical and biophysical research communications Abstract HTLV1 I334A 52 57 gp21;gp21 112;194 116;198 17609263 The role of WWP1-Gag interaction and Gag ubiquitination in assembly and release of human T-cell leukemia virus type 1. Furthermore, the K74R mutation rendered assembly hypersensitive to C2WW inhibition; K74R Gag budding was inhibited at significantly lower levels of expression of C2WW compared with wild-type Gag. 2007 Journal of virology Abstract HTLV1 K74R;K74R 17;84 21;88 Gag;Gag 89;191 92;194 17609263 The role of WWP1-Gag interaction and Gag ubiquitination in assembly and release of human T-cell leukemia virus type 1. Virus-like particles produced by the K74R mutant did not contain ubiquitinated MA and showed a fourfold reduction in the release of infectious particles. 2007 Journal of virology Abstract HTLV1 K74R 37 41 18480461 Intersubunit disulfide isomerization controls membrane fusion of human T-cell leukemia virus Env. However, the rearrangement was blocked by the C225A mutation, suggesting that C(225) carried the isomerization-active thiol. 2008 Journal of virology Abstract HTLV1 C225A 46 51 18480461 Intersubunit disulfide isomerization controls membrane fusion of human T-cell leukemia virus Env. Still, it was possible to reduce the intersubunit disulfide of the native C225A ectodomain mutant with dithiothreitol (DTT). 2008 Journal of virology Abstract HTLV1 C225A 74 79 18480461 Intersubunit disulfide isomerization controls membrane fusion of human T-cell leukemia virus Env. The importance of the CXXC-mediated disulfide isomerization for infection was studied using murine leukemia virus vectors pseudotyped with wild-type or C225A HTLV-1 Env. 2008 Journal of virology Abstract HTLV1 C225A 152 157 Env 165 168 18480461 Intersubunit disulfide isomerization controls membrane fusion of human T-cell leukemia virus Env. We introduced the C225A and C228A mutations into Env and found that the former but not the latter mutant matured into covalently linked SU-TM complexes in transfected cells. 2008 Journal of virology Abstract HTLV1 C225A;C228A 18;28 23;33 Env 49 52 20526659 The pleiotropic protein kinase CK2 phosphorylates HTLV-1 Tax protein in vitro, targeting its PDZ-binding motif. We also show that the mutation of Thr-351 to aspartate abolishes Tax-1 binding to the scaffold protein hDlg, a tumour suppressor factor, while having no effect on transactivation. 2010 Virus genes Abstract HTLV1 T351D 34 54 Tax 65 68 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. CONCLUSIONS: The data described here show that changes in domain A of the HTLV-1 TRE-1 motif resulting in the G232A mutation may increase HTLV-1 replication in a majority of infected subjects. 2011 Virology journal Abstract HTLV1 G232A 110 115 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. RESULTS: Using a categorical analysis, a G232A substitution, located in domain A of the TRE-1 motif, was detected in 38.7% (12/31), 27.5% (8/29), and 61.8% (21/34) of subjects with low, intermediate, or high PvLs, respectively. 2011 Virology journal Abstract HTLV1 G232A 41 46 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. This result was confirmed by a non-parametric analysis that showed strong evidence for higher PvLs among HTLV-1 positive individuals with the G232A mutation than those without this mutation (p < 0.03). 2011 Virology journal Abstract HTLV1 G232A 142 147 22947305 LTR point mutations in the Tax-responsive elements of HTLV-1 isolates from HIV/HTLV-1-coinfected patients. described point mutations into Tax-responsive elements (TRE) of the LTR region of HTLV-1 isolates from asymptomatic carriers from Sao Paulo, Brazil, and hypothesized that the presence of the G232A mutation in the TRE-1 increase viral proliferation and consequently the proviral load (PvL), while the A184G mutation in the TRE-2 do not have such effect. 2012 Virology journal Abstract HTLV1 G232A;A184G 191;300 196;305 Tax;LTR 31;68 34;71 22947305 LTR point mutations in the Tax-responsive elements of HTLV-1 isolates from HIV/HTLV-1-coinfected patients. High frequency (13/24, 54.2%) of double mutations G232A and A184G was also detected in HIV/HTLV-1-coinfected patients. 2012 Virology journal Abstract HTLV1 G232A;A184G 50;60 55;65 HTLV1-HIV coinfections 87 108 22947305 LTR point mutations in the Tax-responsive elements of HTLV-1 isolates from HIV/HTLV-1-coinfected patients. The frequency of G232A mutation (16/24, 66.7%) was high as much as 61.8% reported by Neto's in HTLV-1 asymptomatic carriers with high PvL. 2012 Virology journal Abstract HTLV1 G232A 17 22 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. A single amino acid (aa) substitution (S35L) was exclusive for the HC group, and three gp46 substitutions (F14S, N42H, G72S) were exclusive for the HAM/TSP group. 2013 Virology journal Abstract HTLV1 S35L;F14S;N42H;G72S 39;107;113;119 43;111;117;123 gp46 87 91 HTLV-1-associated myelopathy/tropical spastic paraparesis 148 155 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. CONCLUSIONS: The most common gp46 mutations were not associated clinical status because they were found in only one individual, except for the V247I mutation, that was found at viral clones from HAM/TSP ad HC individuals. 2013 Virology journal Abstract HTLV1 V247I 143 148 gp46 29 33 HTLV-1-associated myelopathy/tropical spastic paraparesis 195 202 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. The in silico protein analysis revealed that the mutated alleles F14S and N42H represent more hydrophilic and flexible protein domains that are likely to be less antigenic. 2013 Virology journal Abstract HTLV1 F14S;N42H 65;74 69;78 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. The remaining frequent mutation (V247I) was present in both groups (p = 0.0014). 2013 Virology journal Abstract HTLV1 V247I 33 38 23785214 Human T lymphotropic virus type 1 SU residue 195 plays a role in determining the preferential CD4+ T cell immortalization/transformation tropism. Furthermore, a single amino acid substitution, N195D, in HTLV-1 SU (Ach.195) resulted in a shift to a CD8(+) T cell immortalization tropism preference. 2013 Journal of virology Abstract HTLV1 N195D 47 52 23800288 Molecular study of HBZ and gp21 human T cell leukemia virus type 1 proteins isolated from different clinical profile infected individuals. From 10 HBZ analyzed sequences, two amino acid changes were identified (S9P and T95I) at the activation domain. 2013 AIDS research and human retroviruses Abstract HTLV1 T95I;S9P 80;72 84;75 HBZ 8 11 23800288 Molecular study of HBZ and gp21 human T cell leukemia virus type 1 proteins isolated from different clinical profile infected individuals. From eight gp21-analyzed sequences one amino acid change (Y477H) was associated with the switch of a helix to coil structure at secondary structure prediction. 2013 AIDS research and human retroviruses Abstract HTLV1 Y477H 58 63 gp21 11 15 23800288 Molecular study of HBZ and gp21 human T cell leukemia virus type 1 proteins isolated from different clinical profile infected individuals. One mutation (R112C) located at the nuclear localization signal was present in 66.7% and 25% of healthy carriers (HC) and TSP/HAM groups, respectively. 2013 AIDS research and human retroviruses Abstract HTLV1 R112C 14 19 24284316 Palmitoylation and p8-mediated human T-cell leukemia virus type 1 transmission. However, the ability of p8 to localize to the cell surface and to increase cell adhesion and viral transmission was not affected by the C39A mutation. 2014 Journal of virology Abstract HTLV1 C39A 136 140 24284316 Palmitoylation and p8-mediated human T-cell leukemia virus type 1 transmission. Mutation of cysteine 39 to alanine (C39A) abrogated dimerization and palmitoylation of both proteins. 2014 Journal of virology Abstract HTLV1 C39A;C39A 12;36 34;40 25319617 Molecular insights on analogs of HIV PR inhibitors toward HTLV-1 PR through QM/MM interactions and molecular dynamics studies: comparative structure analysis of wild and mutant HTLV-1 PR. Functional analysis of M37A mutation in HTLV PR clearly shows that the MET37 specificity and screening of potential inhibitors targeting MET37 is performed by using approved 90% similar HIV PR inhibitor compounds. 2014 Journal of molecular recognition Abstract HTLV1 M37A 23 27 PR;PR 45;190 47;192 25830656 The prevalence of human T-lymphotropic virus infection among blood donors in southeast China, 2004-2013. Interestingly, 12 of 25 Transcontinental subtype sequences harbored a characteristic L55P mutation in viral gp46 protein, which was only presented in the Transcontinental subtype sequences from Japan and Taiwan but not in that from other countries. 2015 PLoS neglected tropical diseases Abstract HTLV1 L55P 85 89 gp46 108 112 26472535 Deep Sequencing Analysis of Human T Cell Lymphotropic Virus Type 1 Long Terminal Repeat 5' Region from Patients with Tropical Spastic Paraparesis/Human T Cell Lymphotropic Virus Type 1-Associated Myelopathy and Asymptomatic Carriers. Although those mutations were not present in previously determined TFBS, one of those mutations (G306C/A) was present in an Sp-1 binding site determined by in silico analysis, and its presence abrogated the site for Sp-1 binding and created a new possible ATF binding site. 2016 AIDS research and human retroviruses Abstract HTLV1 G306C;G306A 97;97 104;104 26472535 Deep Sequencing Analysis of Human T Cell Lymphotropic Virus Type 1 Long Terminal Repeat 5' Region from Patients with Tropical Spastic Paraparesis/Human T Cell Lymphotropic Virus Type 1-Associated Myelopathy and Asymptomatic Carriers. Three mutations were statistically significant using the Fisher nonparametric test between the groups but were not present in previously determined TFBS (G126C/T, G306C, and C479T). 2016 AIDS research and human retroviruses Abstract HTLV1 G126C;G126T;C479T;G306C 154;154;174;163 161;161;179;168 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? Mutations in the distal and central regions of Tax Responsive Elements (TRE) 1 and 2 of G3 were observed, though not associated with PVL.The 8403A>G mutation of the distal region, previously related to high PVL, was absent in G3 but present in 50% of WB+ samples (p = 0.03). 2015 Viruses Abstract HTLV1 A8403G 141 148 Tax 47 50 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. Our analyses demonstrated that some mutations may be associated with the outcome of HAM/TSP (C39R, L40F, P45L, S69G and R88K) or with proviral load (P34L and F61L). 2016 Infection, genetics and evolution Abstract HTLV1 C39R;L40F;P45L;S69G;R88K;P34L;F61L 93;99;105;111;120;149;158 97;103;109;115;124;153;162 HTLV-1-associated myelopathy/tropical spastic paraparesis 84 91 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. We further examined the presence of mutations in motifs of HBZ and observed that P45L mutation is located within the HBZ nuclear localization signal and was found more frequently between patients with HAM/TSP and high proviral load. 2016 Infection, genetics and evolution Abstract HTLV1 P45L 81 85 HBZ;HBZ 59;117 62;120 HTLV-1-associated myelopathy/tropical spastic paraparesis 201 208 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. Of the three most frequent mutations, the previously undescribed N93D mutant was invariably associated with symptomatic cases. 2018 Virology journal Abstract HTLV1 N93D 65 69 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. The identification of a rare mutation (N93D), present only in symptomatic patients, should also be investigated further as a potential clinical marker. 2018 Virology journal Abstract HTLV1 N93D 39 43 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. The rare N93D amino acid mutation may be associated with the clinical manifestations of this viral infection. 2018 Virology journal Abstract HTLV1 N93D 9 13 31299491 The human T-cell leukemia virus type-1 tax oncoprotein dissociates NF-kappaB p65(RelA)-Stathmin complexes and causes catastrophic mitotic spindle damage and genomic instability. The Tax-G148V mutant, defective for NF-kappaB activation, exhibited reduced p65RelA-Stathmin binding and diminished genomic instability and cytotoxicity. 2019 Virology Abstract HTLV1 G148V 8 13 Tax 4 7 33539355 Prevalence and evolutionary analyses of human T-cell lymphotropic virus in Guangdong province, China: Transcontinental and Japanese subtype lineages dominate the prevalence. Specially, 13 out of 39 transcontinental subtype sequences were characterized with L55P mutation and 21 out of 55 sequences were characterized with L19F mutation in viral gp46 protein. 2021 PLoS neglected tropical diseases Abstract HTLV1 L55P;L19F 83;148 87;152 gp46 171 175 33539355 Prevalence and evolutionary analyses of human T-cell lymphotropic virus in Guangdong province, China: Transcontinental and Japanese subtype lineages dominate the prevalence. The L55P mutation seemed be specific to eastern Asia since it only presented in the sequences from Japan, mainland China, and Taiwan. 2021 PLoS neglected tropical diseases Abstract HTLV1 L55P 4 8 33835501 Molecular characterization of HTLV-1 genomic region hbz from patients with different clinical conditions. The analises showed that the R119Q mutation seems to be related to HTLV-1 clinical conditions since the frequency of this HBZ mutation is significantly different in comparison between AC with HAM/TSP and ATLL. 2021 Journal of medical virology Abstract HTLV1 R119Q 29 34 HBZ 122 125 T-cell leukemia/lymphoma;HTLV-1-associated myelopathy/tropical spastic paraparesis 204;192 208;199 33835501 Molecular characterization of HTLV-1 genomic region hbz from patients with different clinical conditions. The R119Q mutation is possibly a protective factor as the frequency is higher in AC sequences. 2021 Journal of medical virology Abstract HTLV1 R119Q 4 9 34343702 The N93D mutation of the human T-cell leukemia virus type 1 envelope glycoprotein found in symptomatic patients enhances neuropilin-1 b1 domain binding. However, it remains unclear how the SU-N93D mutation affects Nrp1 b1 binding. 2021 Biochimica et biophysica acta. Proteins and proteomics Abstract HTLV1 N93D 39 43 34343702 The N93D mutation of the human T-cell leukemia virus type 1 envelope glycoprotein found in symptomatic patients enhances neuropilin-1 b1 domain binding. Our results suggest that the interaction of SU Asp93 with the four residues of Nrp1 b1 renders the high affinity of the N93D mutant for Nrp1 b1 binding during HTLV-1 entry. 2021 Biochimica et biophysica acta. Proteins and proteomics Abstract HTLV1 N93D 120 124 34343702 The N93D mutation of the human T-cell leukemia virus type 1 envelope glycoprotein found in symptomatic patients enhances neuropilin-1 b1 domain binding. Recently, the N93D mutation in the Nrp1 b1 binding region of the SU was identified in symptomatic patients with HTLV-1 infections in the Brazilian Amazon. 2021 Biochimica et biophysica acta. Proteins and proteomics Abstract HTLV1 N93D 14 18 HTLV-1 infections 112 129 34343702 The N93D mutation of the human T-cell leukemia virus type 1 envelope glycoprotein found in symptomatic patients enhances neuropilin-1 b1 domain binding. The SU-N93D peptide binds directly to Nrp1 b1 with a binding affinity of 3.5 muM, which is approximately two-fold stronger than wild-type. 2021 Biochimica et biophysica acta. Proteins and proteomics Abstract HTLV1 N93D 7 11 34343702 The N93D mutation of the human T-cell leukemia virus type 1 envelope glycoprotein found in symptomatic patients enhances neuropilin-1 b1 domain binding. This stronger binding is likely a result of the interaction between the substituted residue Asp93 of the N93D peptide and the four residues Trp301, Lys347, Glu348, and Thr349 of Nrp1 b1. 2021 Biochimica et biophysica acta. Proteins and proteomics Abstract HTLV1 N93D 105 109 34343702 The N93D mutation of the human T-cell leukemia virus type 1 envelope glycoprotein found in symptomatic patients enhances neuropilin-1 b1 domain binding. To elucidate the impact of the substituted Asp93 of SU on Nrp1 b1 binding, we analyzed the interaction between the SU-N93D peptide and Nrp1 b1 using isothermal titration calorimetry and nuclear magnetic resonance. 2021 Biochimica et biophysica acta. Proteins and proteomics Abstract HTLV1 N93D 118 122 34494950 Polymorphisms in HTLV-1 Tax-responsive elements in HTLV-1-associated myelopathy/tropical spastic paraparesis patients are associated with reduced proviral load but not with disease progression. By contrast, an LTR A125G mutation in TRE was associated with slightly reduced PVL only in HAM/TSP patients, although it did not influence the speed of disease progression. 2021 The Journal of general virology Abstract HTLV1 A125G 20 25 LTR 16 19 HTLV-1-associated myelopathy/tropical spastic paraparesis 91 98 8756622 Interaction of the human T-cell lymphotropic virus type 1 tax transactivator with transcription factor IIA. Importantly, two previously characterized mutants with point mutations in Tax, M32 (Y196A, K197S) and M41 (H287A, P288S), which were shown to be defective in Tax-activated transcription were unable to interact with TFIIA in this assay. 1996 Molecular and cellular biology Abstract HTLV1 Y196A;K197S;H287A;P288S 84;91;107;114 89;96;112;119 Tax;Tax 74;158 77;161 8970957 Interaction of the human T-lymphotropic virus type 1 Tax dimer with CREB and the viral 21-base-pair repeat. A dual amino acid substitution mutant of Tax, M47 (L319R, L320S), completely abrogated for activation of the human T-lymphotropic virus type 1 long terminal repeat as a result of a defect in the transactivation domain, continues to stimulate binding of bZip proteins to DNA. 1996 Journal of virology Abstract HTLV1 L319R;L320S 51;58 56;63 Tax 41 44 9131461 Common origin of human T-lymphotropic virus type-I from Iran, Kuwait, Israel, and La Reunion Island. All seven isolates were positive for T-->C 4783 and six, from which env fragment was amplifiable, were also positive for T-->C 6569. 1997 Journal of medical virology Abstract HTLV1 T4783C;T6569C 37;121 47;131 Env 68 71 9131461 Common origin of human T-lymphotropic virus type-I from Iran, Kuwait, Israel, and La Reunion Island. It is highly probable that all the isolates from Mashhadi Jews belong to the same HTLV-I lineage, although they were not typed yet for the presence of T-->C 6569 substitution. 1997 Journal of medical virology Abstract HTLV1 T6569C 151 161 9131461 Common origin of human T-lymphotropic virus type-I from Iran, Kuwait, Israel, and La Reunion Island. The determination of the T-->C 4783 and T-->C 6569 markers in HTLV-I isolates of different geographical/ethnic origin may be useful for the reconstruction of the routes of HTLV-I spread from the Middle East and/or Indian subcontinent to other regions of the world and, possibly, for gaining insights into the origin of HTLV-I in Asia. 1997 Journal of medical virology Abstract HTLV1 T4783C;T6569C 25;40 35;50 9131461 Common origin of human T-lymphotropic virus type-I from Iran, Kuwait, Israel, and La Reunion Island. We found previously that Kuwaiti HTLV-I isolates had two nucleotide substitutions in the most frequently sequenced regions of HTLV-I genome, namely: T-->C 4783 in the pol and T-->C 6569 the env genes. 1997 Journal of medical virology Abstract HTLV1 T4783C;T6569C 149;175 159;185 Pol;Env 167;190 170;193 9710589 An exposed KID-like domain in human T-cell lymphotropic virus type 1 Tax is responsible for the recruitment of coactivators CBP/p300. Site-directed mutagenesis of residues in this domain (R82A, K85A, K88A, and V89A) resulted in proteins which failed to transactivate from the HTLV-1 LTR in vivo. 1998 Molecular and cellular biology Abstract HTLV1 R82A;K85A;K88A;V89A 54;60;66;76 58;64;70;80 LTR 149 152 9710589 An exposed KID-like domain in human T-cell lymphotropic virus type 1 Tax is responsible for the recruitment of coactivators CBP/p300. These mutants (K85A, K88A, and V89A) bind CREB with similar affinities as wild-type Tax, yet interaction with CBP/p300 is abrogated in various biochemical assays, indicating that the recruitment of CBP/p300 is crucial for Tax transactivation. 1998 Molecular and cellular biology Abstract HTLV1 K85A;K88A;V89A 15;21;31 19;25;35 Tax;Tax 84;222 87;225 9765430 Human T-cell lymphotropic/leukemia virus type 1 Tax abrogates p53-induced cell cycle arrest and apoptosis through its CREB/ATF functional domain. The Tax mutants M22 and G148V, which selectively activate the CREB/ATF pathway, exert these same biological effects on p53 function. 1998 Journal of virology Abstract HTLV1 G148V 24 29 Tax 4 7 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. C23W, A108T, L159F, and L235F transactivated both the HTLV-LTR and the NF-kappaB reporters. 2007 Retrovirology Introduction HTLV1 C23W;A108T;L159F;L235F 0;6;13;24 4;11;18;29 LTR 59 62 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Five mutants (V19M, C23W, A108T, L159F, and L235F) - with amino acid substitutions that span the majority of Tax protein sequence - were chosen for in-depth analyses. 2007 Retrovirology Introduction HTLV1 V19M;C23W;A108T;L159F;L235F 14;20;26;33;44 18;24;31;38;49 Tax 109 112 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. One mutant, V19M, preferentially activated NF-kappaB, but was attenuated in LTR activation. 2007 Retrovirology Introduction HTLV1 V19M 12 16 LTR 76 79 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? have reported an association between G232A in the Tax Responsive Element (TRE) 1 and an increase in PVL levels. 2015 Viruses Introduction HTLV1 G232A 37 42 Tax 50 53 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. demonstrated two natural allelic variants of p12: a lysine-to-arginine change at position 88, which was found more frequently in patients with HAM/TSP and could be important for HTLV-1 outcome. 2016 Infection, genetics and evolution Introduction HTLV1 K88R 52 92 P12 45 48 HTLV-1-associated myelopathy/tropical spastic paraparesis 143 150 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Transactivation functions of V19M, C23W, A108T, L159F, and L235F mutants were further confirmed by including in the transfection mixture 0.5 mug of a control plasmid, pRL-TK, that contains the renilla luciferase reporter gene driven by the herpesvirus thymidine kinase promoter. 2007 Retrovirology Method HTLV1 V19M;C23W;A108T;L159F;L235F 29;35;41;48;59 33;39;46;53;64 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. We selected the most frequent natural mutations within ORF-I sequences (F3L, S23P, D26N, G29S, P34L, C39R, L40F, P45L, F61L, S63P, L66P, S69G, R83C, R88K and P91S) to evaluate their possible association with the development of HAM/TSP using the Excel program. 2016 Infection, genetics and evolution Method HTLV1 F3L;S23P;D26N;G29S;P34L;C39R;L40F;P45L;F61L;S63P;L66P;S69G;R83C;R88K;P91S 72;77;83;89;95;101;107;113;119;125;131;137;143;149;158 75;81;87;93;99;105;111;117;123;129;135;141;147;153;162 ORF-I 55 60 HTLV-1-associated myelopathy/tropical spastic paraparesis 227 234 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Approximately half of the mutants analyzed (S32F, A47T, H52Y, G61E, L75F, T145I, W147L, P169L, A285T, and S300F) were greatly impaired in both transactivation functions of Tax. 2007 Retrovirology Result HTLV1 S32F;A47T;H52Y;G61E;L75F;T145I;W147L;P169L;A285T;S300F 44;50;56;62;68;74;81;88;95;106 48;54;60;66;72;79;86;93;100;111 Tax 172 175 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. As indicated below, at least five of these mutants (V19M, C23W, A108T, L159F, and L235F) expressed at levels comparable to that of the wild-type Tax in HeLa cells (see below). 2007 Retrovirology Result HTLV1 V19M;C23W;A108T;L159F;L235F 52;58;64;71;82 56;62;69;76;87 Tax 145 148 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. By contrast, several mutants (C23W, P102L, A108T, A108V, H127T, L159F, 235F, G245D, and D264Y) continued to transactivate both LTR and NF-kappaB reporters to levels (greater than 50%) comparable to those of the wild-type Tax. 2007 Retrovirology Result HTLV1 C23W;P102L;A108T;A108V;H127T;L159F;G245D;D264Y 30;36;43;50;57;64;77;88 34;41;48;55;62;69;82;93 Tax;LTR 221;127 224;130 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. By contrast, the morphology of cells transduced with mutant tax alleles, with the exception of A108T, resembled those of control cells transduced with the EGFP gene. 2007 Retrovirology Result HTLV1 A108T 95 100 Tax 60 63 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. By contrast, the S. cerevisiae-viable V19M, C23W, A108T, L159F, and L235F tax mutants were attenuated in causing Clb2p reduction/degradation. 2007 Retrovirology Result HTLV1 V19M;C23W;A108T;L159F;L235F 38;44;50;57;68 42;48;55;62;73 Tax 74 77 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Consistent with the notion that the amino acid substitutions had occurred in important regions of Tax, we noticed that the T130I substitution overlap with the dual amino acid substitutions - T130A L131S - in a well characterized tax mutant known as M22, which is partially defective in dimerization and is severely impaired in IKKgamma/NEMO-binding and NF-kappaB activation. 2007 Retrovirology Result HTLV1 T130I;T130A;L131S 123;191;197 128;196;202 Tax;Tax 98;229 101;232 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Drug-resistant colonies were then grown in puromycin-free medium for 1 day and observed under a fluorescence microscope for DsRed expression. In agreement with the LTR-Luc reporter activities described above (Fig,2), C23W, A108T, L159F, and L235F, but not V19M activated DsRed expression聽鈥(Fig.3B). 2007 Retrovirology Result HTLV1 C23W;A108T;L159F;L235F;V19M 217;223;230;241;256 221;228;235;246;261 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Finally, the degrees of the mutants to cause cyclin B1 polyubiquitination (A108T >= C23W > L159F, L235F, and V19M) correlated largely with the levels of p21CIP1/WAF1and p27KIP 1increase in the transduced cells (A108T > C23W > L159F, L235F, and V19M). 2007 Retrovirology Result HTLV1 A108T;C23W;L159F;L235F;V19M;A108T;C23W;L159F;L235F;V19M 75;84;91;98;109;211;219;226;233;244 80;88;96;103;113;216;223;231;238;248 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Finally, we noted that despite some similarity of A108T cells to Tax (wild-type) cells, the extent of arrest and morphological changes in A108T cells appeared to be attenuated. 2007 Retrovirology Result HTLV1 A108T;A108T 50;138 55;143 Tax 65 68 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. HeLa-18 x 21-DsRed cells were infected with LV carrying the wild-type, V19M, C23W, A108T, L159F, L235F tax alleles, or the EGFP gene. 2007 Retrovirology Result HTLV1 V19M;C23W;A108T;L159F;L235F 71;77;83;90;97 75;81;88;95;102 Tax 103 106 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Here again, in general agreement with the reporter assays, the A108T mutant is equivalent or possibly better than the wild-type tax in inducing I-kappaBalpha degradation and p52 NF-kappaB processing, second by V19M and C23W, followed lastly by L235F and L159 mutants. 2007 Retrovirology Result HTLV1 A108T;V19M;C23W;L235F 63;210;219;244 68;214;223;249 Tax 128 131 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. In accordance with the overall cell morphology and flow cytometry analyses, the levels of p21CIP1/WAF1and p27KIP 1in the various tax-transduced cells correlated with their extent of growth arrest or lack thereof, with wild-type tax greatly increasing the levels of p21CIP1/WAF1and p27KIP1, followed by the A108T mutant, and with the remaining mutants having only moderate to no effect (C23W, L159F, L235F, V19M). 2007 Retrovirology Result HTLV1 A108T;C23W;L159F;L235F;V19M 306;386;392;399;406 311;390;397;404;410 Tax;Tax 129;228 132;231 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Of note, V19M was specifically impaired in LTR activation but remained a potent NF-kappaB activator, while T130I was defective in NF-kappaB activation, but exhibited significant LTR activation capability, reminiscent of similar properties of the M22 (T130A L131S) mutation mentioned above. 2007 Retrovirology Result HTLV1 T130A;L131S;V19M;T130I 251;257;9;107 256;262;13;112 LTR;LTR 43;178 46;181 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. The other five mutants (V24E, C36Y, G61R, P92L, and L183F) were excluded from the reporter assays because of either the drastic amino acid alterations caused by the mutations or the existence of alternative amino acid substitution in the same position. 2007 Retrovirology Result HTLV1 V24E;C36Y;G61R;P92L;L183F 24;30;36;42;52 28;34;40;46;57 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Two distinct mutations (G61E and G61R) and (A108T and A108V) were isolated for each of the amino acid residues 61 and 108, suggesting the importance of these residues in protein-protein interactions that mediate Tax functions. 2007 Retrovirology Result HTLV1 G61E;G61R;A108T;A108V 24;33;44;54 28;37;49;59 Tax 212 215 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. We next selected 5 mutants (V19M, C23W, A108T, L159F, and L235F) that retained the ability to transactivate LTR and/or NF-kappaB for further analysis. 2007 Retrovirology Result HTLV1 V19M;C23W;A108T;L159F;L235F 28;34;40;47;58 32;38;45;52;63 LTR 108 111 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. While for some mutants (A108T, L159F, and L235F) there appears to be some correlation between the severity of cell cycle arrest/senescence phenotype and the degree of NF-kappaB activation, for others such as V19M and C23W, that are strong NF-kappaB activators, the senescence phenotype was significantly attenuated. 2007 Retrovirology Result HTLV1 A108T;L159F;L235F;V19M;C23W 24;31;42;208;217 29;36;47;212;221 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. A significant difference in detection of the G232A mutation was found between subjects with high and low PvLs and between those with high and intermediate PvLs (p < 0.05 both). 2011 Virology journal Result HTLV1 G232A 45 50 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. Again, a significant difference in detection of the A184G mutation was evident between subjects with high and low PvLs and betweeen those with high and intermediate PvLs (p < 0.05 both), but not between the low and intermediate PvL groups (p > 0.05). 2011 Virology journal Result HTLV1 A184G 52 57 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. Because these two analyses did not reach the same conclusion, we considered only G232A as a potential mutation that could impact patient PvL. 2011 Virology journal Result HTLV1 G232A 81 86 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. The distributions of this mutation according to PvL groups was similar to the frequency of the G232A mutation being found in 38.7% (12/31) in subjects with a low PvL, 20.7% (6/29) in subjects with an intermediate PvL, and 52.9% (18/34) in subjects with a high PvL. 2011 Virology journal Result HTLV1 G232A 95 100 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. The G232A mutation was detected in 38.7% (12/31) of subjects with a low PvL, 27.5% (8/29) of subjects with an intermediate PvL, and 61.8% (21/34) of subjects with a high PvL (Table 1). 2011 Virology journal Result HTLV1 G232A 4 9 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. there was no similar association among those who were HTLV-1 positive with the A184G mutation (Figure 2). 2011 Virology journal Result HTLV1 A184G 79 84 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. These analyses revealed two relevant G232A mutation within the TRE-1 region and an A184G mutation within the TRE-2 region numbered according to the transcription start site. 2011 Virology journal Result HTLV1 G232A;A184G 37;83 42;88 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. Thirty-six of 41 (87.8%) HTLV-1 G232A mutations were associated with a simultaneous A to G mutation at position 184 (Figure 1). 2011 Virology journal Result HTLV1 G232A;A184G 32;84 37;115 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. This analysis revealed that while there was strong evidence for a higher PvL among HTLV-1 positive individuals with the G232A mutation than those without this mutation (42.2 vs. 2011 Virology journal Result HTLV1 G232A 120 125 22947305 LTR point mutations in the Tax-responsive elements of HTLV-1 isolates from HIV/HTLV-1-coinfected patients. Furthermore, 13 subjects (54.2%) had double mutations of the TRE-1 G232A and the TRE-2 A184G, three (12.5%) had the TRE-1 G232A mutation only, none had the TRE-2 A184G mutation only, and eight (33.3%) had no mutation in both sites. 2012 Virology journal Result HTLV1 G232A;A184G;G232A;A184G 67;87;122;162 72;92;127;167 22947305 LTR point mutations in the Tax-responsive elements of HTLV-1 isolates from HIV/HTLV-1-coinfected patients. In the December 13th, 2011 issue of Virology Journal, Neto and collaborators described point mutations into 21-bp repeat motifs, named Tax-responsive elements (TRE), present in the 5' LTR region of human T-lymphotropic virus type 1 (HTLV-1) isolated among asymptomatic carriers from Sao Paulo, Brazil, and hypothesized that the presence of G232A nucleotide substitution in the A domain of the first TRE (TRE-1) increase viral proliferation and consequently the proviral load (PvL), while the A184G mutation in the A domain of TRE-2 do not have such effect. 2012 Virology journal Result HTLV1 G232A;A184G 340;492 345;497 5'LTR;Tax 181;135 187;138 22947305 LTR point mutations in the Tax-responsive elements of HTLV-1 isolates from HIV/HTLV-1-coinfected patients. Of 24 subjects, the TRE-1 G232A mutation was detected in 16 (66.7%) and the TRE-2 A184G mutation in 13 (54.2%). 2012 Virology journal Result HTLV1 G232A;A184G 26;82 31;87 22947305 LTR point mutations in the Tax-responsive elements of HTLV-1 isolates from HIV/HTLV-1-coinfected patients. The frequency of the substitution A G in the second nucleotide (A domain) of the TRE-1 motif (the TRE-1 G232A mutation) and the substitution G A in the third nucleotide (A domain) of the TRE-2 motif (the TRE-2 A184G mutation) was summarized in Table 1. 2012 Virology journal Result HTLV1 G232A;A184G 106;214 111;219 22947305 LTR point mutations in the Tax-responsive elements of HTLV-1 isolates from HIV/HTLV-1-coinfected patients. The frequency of the TRE-1 G232A mutation (66.7%) in HIV/HTLV-1-coinfected patients was high as much as 61.8% reported by Neto's in HTLV-1 asymptomatic carriers with a high PvL. 2012 Virology journal Result HTLV1 G232A 27 32 HTLV1-HIV coinfections 53 74 22947305 LTR point mutations in the Tax-responsive elements of HTLV-1 isolates from HIV/HTLV-1-coinfected patients. Thus, all the 13 subjects with the TRE-2 A184G mutation had the TRE-1 G232A mutation together. 2012 Virology journal Result HTLV1 A184G;G232A 41;70 46;75 22947305 LTR point mutations in the Tax-responsive elements of HTLV-1 isolates from HIV/HTLV-1-coinfected patients. We also found that the frequency of double mutations of the TRE-1 G232A and the TRE-2 A184G in HIV/HTLV-1-coinfected was high (54.2%). 2012 Virology journal Result HTLV1 G232A;A184G 66;86 71;91 HTLV1-HIV coinfections 95 116 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. According to our results, other less frequent mutations were associated to changes in the physico-chemical profile and potential protein domains: the T142I mutation was associated to the loss of a N-glycosylation site and to a decrease in antigenicity; the F159S mutation presented a more hydrophilic and flexible profile, associated to the insertion of a N-Myristilation site; and the H290D, C289R and F141S mutations were characterized by an increase in hydrophilicity and flexibility, the opposite of the D197N mutation which was associated to a decrease in flexibility (Data not shown). 2013 Virology journal Result HTLV1 T142I;F159S;H290D;C289R;F141S;D197N 150;257;386;393;403;508 155;262;391;398;408;513 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. After submission of wild type and mutated sequences to SWISS-MODEL server, the results showed that the S35L and G72S mutations were associated to the change of coil for extended beta at the secondary structure prediction (Figure 5). 2013 Virology journal Result HTLV1 S35L;G72S 103;112 107;116 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. Among the five mutations found, three (F14S, S35L and N42H) were not present in any of the 42 Brazilian sequences used to create the consensus. 2013 Virology journal Result HTLV1 F14S;S35L;N42H 39;45;54 43;49;58 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. Among these common mutations, one (S35L) was exclusive to the HC group, three (F14S, N42H, G72S) were exclusive to the HAM/TSP group and, finally, one mutation (V247I) was found in both groups but with a statistically significant difference in the frequency within the groups (Fisher Test, p = 0.0014). 2013 Virology journal Result HTLV1 S35L;F14S;N42H;G72S;V247I 35;79;85;91;161 39;83;89;95;166 HTLV-1-associated myelopathy/tropical spastic paraparesis 119 126 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. Finally, the V247I mutation was found in sequences from all different geographic regions represented in our dataset. 2013 Virology journal Result HTLV1 V247I 13 18 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. G72S was found in one Brazilian sequence; however, we do not have information about the geographic region from which the sequence was obtained. 2013 Virology journal Result HTLV1 G72S 0 4 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. Moreover, one HAM/TSP sequence was mutated (Y80C) at position 80 aa, which is part of the YSLY motif involved in the protein trafficking to the plasma membrane. 2013 Virology journal Result HTLV1 Y80C 44 48 HTLV-1-associated myelopathy/tropical spastic paraparesis 14 21 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. Similarly, F14S, S35L, N42H and V247I mutations were not present in any sequence of the Cosmopolita dataset, while G72S mutation was found in sequences from Gabon, Martinique, French Guyana and Guadalupe. 2013 Virology journal Result HTLV1 F14S;S35L;N42H;V247I;G72S 11;17;23;32;115 15;21;27;37;119 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. Since the G72S mutation is located in the 53-75 aa domain, we tested both wild type and mutated alleles. 2013 Virology journal Result HTLV1 G72S 10 14 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. The 197 amino acid site, which was already associated to the decrease in cellular fusion, was mutated (D197N) in two clone sequences in our data set: one from the HC group and the other from the HAM/TSP group (data not shown). 2013 Virology journal Result HTLV1 D197N 103 108 HTLV-1-associated myelopathy/tropical spastic paraparesis 195 202 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. The following was observed: 1) the mutated allele presenting the F14S mutation was more hydrophilic and flexible than the wild type allele (Figure 4A); 2) the mutated allele presenting the N42H mutation was less antigenic than the wild type allele (Figure 4B); 3) the mutated allele presenting the V247I mutation was less antigenic than the wild type allele (Figure 4C). 2013 Virology journal Result HTLV1 F14S;N42H;V247I 65;189;298 69;193;303 25830656 The prevalence of human T-lymphotropic virus infection among blood donors in southeast China, 2004-2013. A characteristic L55P mutation in the receptor binding domain (RBD) of gp46 protein was presented in 12 sequences (48.0%) of Transcontinental subtype. 2015 PLoS neglected tropical diseases Result HTLV1 L55P 17 21 gp46 71 75 25830656 The prevalence of human T-lymphotropic virus infection among blood donors in southeast China, 2004-2013. The comparison indicated that the L55P mutation was only observed in Transcontinental subtype strains originated from Japan (9/20, 45.0%), Taiwan (4/11, 36.4%) and China (1/2, 50%), but not appeared in strains isolated from Transcontinental subtype strains originated from other Asia countries (0/3), Africa (0/6), Central America (0/29), Europe (0/22), North America (0/12), South America (0/38), but also in other subtypes of genotype A (0/67) or genotype B/C (0/40). 2015 PLoS neglected tropical diseases Result HTLV1 L55P 34 38 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? Regarding the TRE-2, two punctual mutations (8522T>C, 8545G>A) were observed in sample N 50, while the other three were present in most Argentine sequences. 2015 Viruses Result HTLV1 T8522C;G8545A 45;54 52;61 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? The remaining mutations (H43P and M154V) were detected in sequences N 46 and 47, respectively; H43P is located within the Nuclear Localization Signal domain, the Zn Finger, and CREB activation by Tax, while M154V is in the NF-kB activation region and the Dimerization Domain. 2015 Viruses Result HTLV1 H43P;M154V;H43P;M154V 25;34;96;208 29;39;100;213 Tax 197 200 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? Through the analysis of non-synonymous (NS) mutations in functional domains of the Tax protein, four amino acidic mutations were detected, two of them corresponding to geographical subtypes (A221V, S304N). 2015 Viruses Result HTLV1 A221V;S304N 191;198 196;203 Tax 83 86 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? While not found in any of the LTR sequences from G3, a mutation was observed in the distal region of TRE-1 (8403A>G) in 50% of the remaining sequences, which corresponded to samples with positive HTLV-1 results by WB and a significant difference (p = 0.03) between these frequencies was established. 2015 Viruses Result HTLV1 A8403G 108 115 LTR 30 33 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. A combined classification of proviral load and clinical diagnosis reveals mutations D26N and F61L are associated with low proviral load and HC, whereas mutations S63P and R83C are associated with high proviral load and HAM/TSP (Figure 1C). 2016 Infection, genetics and evolution Result HTLV1 D26N;F61L;S63P;R83C 84;93;162;171 88;97;166;175 HTLV-1-associated myelopathy/tropical spastic paraparesis 219 226 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. Among them, only the P45L mutation is located within the motif previously described (HBZ nuclear localization signal) and was found more frequently between patients with HAM/TSP and high proviral load. 2016 Infection, genetics and evolution Result HTLV1 P45L 21 25 HBZ 85 88 HTLV-1-associated myelopathy/tropical spastic paraparesis 170 177 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. As shown in Figure 1A, mutations P45L, S69G and R88K were found more frequently in patients with a positive diagnosis for HAM/TSP, whereas mutations C39R and L40F were found more frequently in HC. 2016 Infection, genetics and evolution Result HTLV1 P45L;S69G;R88K;C39R;L40F 33;39;48;149;158 37;43;52;153;162 HTLV-1-associated myelopathy/tropical spastic paraparesis 122 129 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. First, Bayesian network analysis with all sequences showed a central association among disease progression, proviral load and patient origin, that interacted directly with mutations in ORF-I region: D26N, G29S, P34L, L40F, P45L, S63P, L66P, S69G, R83C. 2016 Infection, genetics and evolution Result HTLV1 D26N;G29S;P34L;L40F;P45L;S63P;L66P;S69G;R83C 199;205;211;217;223;229;235;241;247 203;209;215;221;227;233;239;245;251 ORF-I 185 190 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. Here, we further examined the presence of these mutations in motifs of HBZ and only four mutations in ORF-I resulted in changes in the HBZ ORF: P34L, P45L, L66P and R88K. 2016 Infection, genetics and evolution Result HTLV1 P34L;P45L;L66P;R88K 144;150;156;165 148;154;160;169 ORF-I;HBZ;HBZ 102;71;135 107;74;138 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. However, as seen in Figure 1B, there was a higher frequency of P34L sequences in individuals with low proviral load. 2016 Infection, genetics and evolution Result HTLV1 P34L 63 67 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. In contrast, mutations D26N, P34L, C39R, F61L and R83C were associated with low proviral load and P45L with high proviral load (Figure 1B). 2016 Infection, genetics and evolution Result HTLV1 D26N;P34L;C39R;F61L;R83C;P45L 23;29;35;41;50;98 27;33;39;45;54;102 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. Similarly, mutations C39R and F61L were more frequently found in patients with low proviral load (Figure 1B). 2016 Infection, genetics and evolution Result HTLV1 C39R;F61L 21;30 25;34 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. The mutations P34L and S91P appear most frequently (>than 40% of the sequences analysed) but are not associated with the development of HAM/TSP. 2016 Infection, genetics and evolution Result HTLV1 P34L;S91P 14;23 18;27 HTLV-1-associated myelopathy/tropical spastic paraparesis 136 143 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. These three mutations (P34L, C39R and F61L) that result in predominant expression of p12 are associated with low proviral load. 2016 Infection, genetics and evolution Result HTLV1 P34L;C39R;F61L 23;29;38 27;33;42 P12 85 88 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. We analysed the presence or absence of fifteen amino acid changes (F3L, S23P, D26N, G29S, P34L, C39R, L40F, P45L, F61L, S63P, L66P, S69G, R83C, R88K and P91S) that influence the expression profile of the HTLV-1 ORF-I protein product. 2016 Infection, genetics and evolution Result HTLV1 F3L;S23P;D26N;G29S;P34L;C39R;L40F;P45L;F61L;S63P;L66P;S69G;R83C;R88K;P91S 67;72;78;84;90;96;102;108;114;120;126;132;138;144;153 70;76;82;88;94;100;106;112;118;124;130;136;142;148;157 ORF-I 211 216 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. We observed several interactions associated with a true positive rate of 0.63 for HAM/TSP, as among D26N mutation and high proviral load or interactions between high proviral load, 26D, 29G and 34P. 2016 Infection, genetics and evolution Result HTLV1 D26N 100 104 HTLV-1-associated myelopathy/tropical spastic paraparesis 82 89 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. Whereas, the mutation D26N, the only mutation that resulted in predominant p8 expression, was not associated with the development of HAM/TSP but was associated with low proviral load and HC (Figure 1B and 1C). 2016 Infection, genetics and evolution Result HTLV1 D26N 22 26 HTLV-1-associated myelopathy/tropical spastic paraparesis 133 140 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. While this mutation was found more frequently in HAM/TSP patients than HC, we did not find a correlation between R88K and proviral load (Figure 1B). 2016 Infection, genetics and evolution Result HTLV1 R88K 113 117 HTLV-1-associated myelopathy/tropical spastic paraparesis 49 56 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. All the cases with the N93D mutation also presented pain, sensitivity, and dysautonomia. 2018 Virology journal Result HTLV1 N93D 23 27 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. Just over half (52.5%; 21) of the 40 samples analyzed in this study presented some type of amino acid mutation, with three types - S72G, N93D and S192P - being recorded most frequently (Table 3). 2018 Virology journal Result HTLV1 S72G;N93D;S192P 131;137;146 135;141;151 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. Six of the 40 samples analyzed in the present study were diagnosed with HAM/TSP, of which, two presented amino acid mutations (one patient with S72G and the other with both L70I and S103P). 2018 Virology journal Result HTLV1 S72G;L70I;S103P 144;173;182 148;177;187 HTLV-1-associated myelopathy/tropical spastic paraparesis 72 79 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. The mutations S72G and N93D were each identified in five samples (23.8% of the total). 2018 Virology journal Result HTLV1 S72G;N93D 14;23 18;27 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. The S192P mutation was recorded in four samples (19.0%), of which two were symptomatic (pain, sensitivity, and dysautonomia), and two were asymptomatic. 2018 Virology journal Result HTLV1 S192P 4 9 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. Three of the five individuals with the S72G mutation were symptomatic, one with HAM/TSP and the other two with pain, sensitivity, and dysautonomia. 2018 Virology journal Result HTLV1 S72G 39 43 HTLV-1-associated myelopathy/tropical spastic paraparesis 80 87 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. While asymptomatic, subject 2454 presented the most amino acid mutations of any individual, with five (S192P, S194 T, L200H, L210H, and L213P). 2018 Virology journal Result HTLV1 S192P;S194T;L200H;L210H;L213P 103;110;118;125;136 108;116;123;130;141 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. In conclusion, the results presented in this study suggest that the most frequent gp46 mutations (F14S, N42H, V247I and S35L), as well as, the mutations (H290D, C289R, F141S, D197N and F159S) associated to the loss of a post-translational site should be evaluated in greater detail, in particular the reactivity of the mutated proteins against natural antibodies. 2013 Virology journal Conclusion HTLV1 F14S;N42H;V247I;S35L;H290D;C289R;F141S;D197N;F159S 98;104;110;120;154;161;168;175;185 102;108;115;124;159;166;173;180;190 gp46 82 86 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? Mutations in LTR and tax have been described among both indeterminate and positive HTLV-1 cases, highlighting 8403A>G in the distal region of TRE-1, already related to high PVL. 2015 Viruses Conclusion HTLV1 A8403G 110 117 Tax;LTR 21;13 24;16 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. The rare mutation N93D was found invariably in patients with oligosymptoms associated with HAM/TSP. 2018 Virology journal Conclusion HTLV1 N93D 18 22 HTLV-1-associated myelopathy/tropical spastic paraparesis 91 98 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. A184G 2011 Virology journal Table HTLV1 A184G 0 5 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. G232A 2011 Virology journal Table HTLV1 G232A 0 5 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 7383C>T 2015 Viruses Table HTLV1 C7383T 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 7398C>T 2015 Viruses Table HTLV1 C7398T 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 7401C>T 2015 Viruses Table HTLV1 C7401T 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 7431G>A 2015 Viruses Table HTLV1 G7431A 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 7448A>C 2015 Viruses Table HTLV1 A7448C 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 7780A>G 2015 Viruses Table HTLV1 A7780G 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 7914T>C 2015 Viruses Table HTLV1 T7914C 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 7920C>T 2015 Viruses Table HTLV1 C7920T 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 7933C>T 2015 Viruses Table HTLV1 C7933T 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 7982C>T 2015 Viruses Table HTLV1 C7982T 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8001A>G 2015 Viruses Table HTLV1 A8001G 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8231G>A 2015 Viruses Table HTLV1 G8231A 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8295G>A 2015 Viruses Table HTLV1 G8295A 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8367C>A 2015 Viruses Table HTLV1 C8367A 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8381G>A 2015 Viruses Table HTLV1 G8381A 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8391G>A 2015 Viruses Table HTLV1 G8391A 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8392G>A 2015 Viruses Table HTLV1 G8392A 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8420C>T 2015 Viruses Table HTLV1 C8420T 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8446G>A 2015 Viruses Table HTLV1 G8446A 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8471G>T 2015 Viruses Table HTLV1 G8471T 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8509A>G 2015 Viruses Table HTLV1 A8509G 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8522T>C 2015 Viruses Table HTLV1 T8522C 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8545G>A 2015 Viruses Table HTLV1 G8545A 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8546T>C 2015 Viruses Table HTLV1 T8546C 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8606C>A 2015 Viruses Table HTLV1 C8606A 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8606C>G 2015 Viruses Table HTLV1 C8606G 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8632G>A 2015 Viruses Table HTLV1 G8632A 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8655G>T 2015 Viruses Table HTLV1 G8655T 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8665C>T 2015 Viruses Table HTLV1 C8665T 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8718C>T 2015 Viruses Table HTLV1 C8718T 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8779T>C 2015 Viruses Table HTLV1 T8779C 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8822G>A 2015 Viruses Table HTLV1 G8822A 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8828A>G 2015 Viruses Table HTLV1 A8828G 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8912T>C 2015 Viruses Table HTLV1 T8912C 0 7 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? 8955G>A 2015 Viruses Table HTLV1 G8955A 0 7 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. C26S 2018 Virology journal Table HTLV1 C26S 0 4 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. F14S 2018 Virology journal Table HTLV1 F14S 0 4 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. I150V 2018 Virology journal Table HTLV1 I150V 0 5 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. L163I 2018 Virology journal Table HTLV1 L163I 0 5 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. L200H 2018 Virology journal Table HTLV1 L200H 0 5 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. L210H 2018 Virology journal Table HTLV1 L210H 0 5 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. L213P 2018 Virology journal Table HTLV1 L213P 0 5 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. L219I 2018 Virology journal Table HTLV1 L219I 0 5 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. L70I 2018 Virology journal Table HTLV1 L70I 0 4 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. N24H 2018 Virology journal Table HTLV1 N24H 0 4 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. N93D 2018 Virology journal Table HTLV1 N93D 0 4 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. S103P 2018 Virology journal Table HTLV1 S103P 0 5 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. S192P 2018 Virology journal Table HTLV1 S192P 0 5 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. S72G 2018 Virology journal Table HTLV1 S72G 0 4 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Morphology of Hela cells transduced with a lentivirus vector carrying, respectively, the wild-type, V19M, C23W, A108T, L159F, and L235F mutant tax alleles. 2007 Retrovirology Figure HTLV1 V19M;C23W;A108T;L159F;L235F 100;106;112;119;130 104;110;117;124;135 Tax 143 146 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. Number of HTLV-1 subjects harboring wild-type or G232A and A184G mutant: viruses correlated with proviral loads. 2011 Virology journal Figure HTLV1 G232A;A184G 49;59 54;64 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. In Figure 4A (F14S), the graphs are organized as follows: hydrophilicity for wild type allele, hydrophilicity for mutated allele, flexibility for wild type allele, and flexibility for the mutated allele. 2013 Virology journal Figure HTLV1 F14S 14 18 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. In Figure 4B (N42H) and 4C (V247I), the graphs are organized as follows: antigenicity for wild type allele and antigenicity for mutated allele. 2013 Virology journal Figure HTLV1 N42H;V247I 14;28 18;33 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. Physico-chemical analysis of wild type and mutated alleles of F14S, N42H and V247I polymorphisms. 2013 Virology journal Figure HTLV1 F14S;N42H;V247I 62;68;77 66;72;82 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. The S35L (A) and G72S (B) polymorphisms were associated to the switch of coil to extended beta structure. 2013 Virology journal Figure HTLV1 S35L;G72S 4;17 8;21 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Both H43Q and M22 are deficient in NF-kappaB but not in LTR transactivation, while K85N is defective for both. 2007 Retrovirology Discussion HTLV1 H43Q;K85N 5;83 9;87 LTR 56 59 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Likewise, several of the mutants - A108T, V19M and C23W, in particular - are potent activators of IKK-NF-kappaB as indicated by luciferase reporter assays and the extent of I-kappaB degradation and p100 processing. 2007 Retrovirology Discussion HTLV1 A108T;V19M;C23W 35;42;51 40;46;55 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Mutants like H43Q and M22, with the possible exception of T130I, however, are not highly represented in the current collection. 2007 Retrovirology Discussion HTLV1 H43Q;T130I 13;58 17;63 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Several tax mutants, H43Q, K85N, and M22 (T130A, L131S) have been shown previously to be disabled for PP2A binding. 2007 Retrovirology Discussion HTLV1 H43Q;K85N;T130A;L131S 21;27;42;49 25;31;47;54 Tax 8 11 17535428 HTLV-1 Tax mutants that do not induce G1 arrest are disabled in activating the anaphase promoting complex. Special attention was directed to five mutants (V19M, C23W, A108T, L159F, and L235F) that remained strong LTR and NF-kappaB transactivators. 2007 Retrovirology Discussion HTLV1 V19M;C23W;A108T;L159F;L235F 48;54;60;67;78 52;58;65;72;83 LTR 106 109 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. Although the functional importance is unclear, it is possible that the G232A mutation in the TRE1 element may enhance indirect binding to Tax via the CREB family of cellular transcription factors, thereby promoting the proliferation of infected cells and resulting in an increase in patient PvLs. 2011 Virology journal Discussion HTLV1 G232A 71 76 Tax 138 141 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. Although the G232A mutation was detected at a higher frequency in asymptomatic HTLV-1 carriers in this study, the frequency of such a mutation is expected to be higher in patients with overt clinical disease, because the PvLs of HTLV-1-infected patients correlates with clinical outcome. 2011 Virology journal Discussion HTLV1 G232A 13 18 HTLV-1 infections 229 244 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. Although the G232A mutation was detected in some subjects with a low PvL in this study, further study is needed to determine if this mutation is predictive of an increase in PvL in patients who possess the mutation but do not have an elevated PvL yet. 2011 Virology journal Discussion HTLV1 G232A 13 18 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. As shown in Figure 1, the G232A and A184G mutations occurred together in almost all instances, most likely because an HTLV strain with both mutations has a higher selective advantage. 2011 Virology journal Discussion HTLV1 G232A;A184G 26;36 31;41 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. However, the validity of this hypothesis needs to be investigated in an independent series of experiments comparing the expression and activation of the Tax gene in HTLV-1-infected T cells with or without the G232A mutation. 2011 Virology journal Discussion HTLV1 G232A 209 214 Tax 153 156 HTLV-1 infections 165 182 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. In conclusion, the results described here suggest the G232A mutation in domain A of the TRE-1 motif may increase HTLV-1 replication in the majority of infected subjects. 2011 Virology journal Discussion HTLV1 G232A 54 59 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. In our study, the G232A mutation was associated with HTLV-1 PvL. 2011 Virology journal Discussion HTLV1 G232A 18 23 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. Interestingly, none of the subjects examined contain only the A184G mutations. 2011 Virology journal Discussion HTLV1 A184G 62 67 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. The G232A mutation is located in domain A of the TRE-1 motif that contains non-consensus CREB response elements and is involved in Tax-activated and basal LTR expression. 2011 Virology journal Discussion HTLV1 G232A 4 9 Tax;LTR 131;155 134;158 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. Therefore, additional experimental supports are needed to rule out the potential importance of the A184G mutations and functional connection between A184G and G232A mutations. 2011 Virology journal Discussion HTLV1 A184G;A184G;G232A 99;149;159 104;154;164 22166003 Correlation between LTR point mutations and proviral load levels among human T cell lymphotropic virus type 1 (HTLV-1) asymptomatic carriers. Therefore, longitudinal study designs are required to address these issues and also to determine if the G232A mutations was already present in patients with advanced disease before they were diagnosed a chronic infection. 2011 Virology journal Discussion HTLV1 G232A 104 109 Advanced disease 157 173 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. Four of the most common mutations (except the V247I mutation) were associated to an intra-host profile because were specifically found in the same single individual: the S35L mutation was exclusive for one HC individual, the F14S and G72S mutations were exclusive for one HAM/TSP individual, and finally the N42H change was exclusive for other HAM/TSP individual. 2013 Virology journal Discussion HTLV1 V247I;S35L;F14S;G72S;N42H 46;170;225;234;308 51;174;229;238;312 HTLV-1-associated myelopathy/tropical spastic paraparesis;HTLV-1-associated myelopathy/tropical spastic paraparesis 272;344 279;351 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. In this regard, three (F14S, S35L and N42H) of these newly identified mutations can be classified as a completely new protein characteristics, while the V247I mutation is an already known characteristic of Brazilian HTLV-1 isolates. 2013 Virology journal Discussion HTLV1 F14S;S35L;N42H;V247I 23;29;38;153 27;33;42;158 23510700 Molecular characterization of HTLV-1 gp46 glycoprotein from health carriers and HAM/TSP infected individuals. The mutations S35L, F14L, G72S and N42H were identified in individuals with high proviral load (log > 5). 2013 Virology journal Discussion HTLV1 S35L;F14L;G72S;N42H 14;20;26;35 18;24;30;39 25830656 The prevalence of human T-lymphotropic virus infection among blood donors in southeast China, 2004-2013. Our results demonstrated the HTLV-1 sequences of Transcontinental subtype in Japan, Taiwan and China shared a unique gp46 L55P mutation which was not presented in sequences originated from other geographic regions. 2015 PLoS neglected tropical diseases Discussion HTLV1 L55P 122 126 gp46 117 121 25830656 The prevalence of human T-lymphotropic virus infection among blood donors in southeast China, 2004-2013. The prevalence in blood donors was 16.9 per 100,000 (95% CI: 12.3-22.8), Ningde people up to 171.3(95% CI: 91.3-292.8); molecular analyses demonstrated most of HTLV-1 isolates (25/27, 92.6%) in our study belong to Transcontinental subtype of genotype A; 12 of 25 Transcontinental subtype sequences harbored a characteristic L55P mutation in viral gp46 protein, which was only presented in the Transcontinental subtype sequences from Japan and Taiwan but not in that from other countries. 2015 PLoS neglected tropical diseases Discussion HTLV1 L55P 324 328 gp46 347 351 25830656 The prevalence of human T-lymphotropic virus infection among blood donors in southeast China, 2004-2013. This frequencies of the L55P mutation among HTLV-1 in Japan, Taiwan and China were very similar (about 36.4-50.0%), that suggested a close relationship in between Transcontinental subtype viral strains of these regions and these viruses possibly shared a common evolutionary ancestor. 2015 PLoS neglected tropical diseases Discussion HTLV1 L55P 24 28 26516904 Low Proviral Load is Associated with Indeterminate Western Blot Patterns in Human T-Cell Lymphotropic Virus Type 1 Infected Individuals: Could Punctual Mutations be Related? Interestingly, we have not observed the 8403A>G mutation (distal region of TRE-1) in any of the G3 sequences, although it was present in 50% of the remaining sequences, all of them positive by WB. 2015 Viruses Discussion HTLV1 A8403G 40 47 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. Despite the high prevalence of P34L mutation and its association with proviral load, this mutation alone could not determine disease. 2016 Infection, genetics and evolution Discussion HTLV1 P34L 31 35 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. Here, we demonstrated only the P45L mutation is located within the HBZ nuclear localization signal and was found more frequently between patients with HAM/TSP and high proviral load. 2016 Infection, genetics and evolution Discussion HTLV1 P45L 31 35 HBZ 67 70 HTLV-1-associated myelopathy/tropical spastic paraparesis 151 158 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. Only R83C mutation is located in a calcineurin-binding motif and is associated with low proviral load. 2016 Infection, genetics and evolution Discussion HTLV1 R83C 5 9 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. Only the data mining approach revealed the coordinate dependency between proviral load, P34L and P45L to be associated with HAM/TSP. 2016 Infection, genetics and evolution Discussion HTLV1 P34L;P45L 88;97 92;101 HTLV-1-associated myelopathy/tropical spastic paraparesis 124 131 27553711 Analyses of HTLV-1 sequences suggest interaction between ORF-I mutations and HAM/TSP outcome. The D26N and F61L mutations are located in the first and second transmembrane domains, respectively, and are found more frequently in patients with low proviral load, as shown in Figure 1B. 2016 Infection, genetics and evolution Discussion HTLV1 D26N;F61L 4;13 8;17 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. (2013) recorded the S72G, N42H and F14S mutations in patients with HAM/TSP. 2018 Virology journal Discussion HTLV1 S72G;N42H;F14S 20;26;35 24;30;39 HTLV-1-associated myelopathy/tropical spastic paraparesis 67 74 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. In the present study, 21 of the samples presented amino acid mutations, of which, S35 L, F14S, and S72G have been described previously, and most are associated with specific functional domains. 2018 Virology journal Discussion HTLV1 S35L;F14S;S72G 82;89;99 87;93;103 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. Subject 2454 presented the most amino acid mutations in its sequence, with five (S192P, S194 T, L200H, L210H, and L213P), but nevertheless remained asymptomatic throughout the study period, which suggests that these changes did not influence the symptomatology of the patient. 2018 Virology journal Discussion HTLV1 S192P;S194T;L200H;L210H;L213P 81;88;96;103;114 86;94;101;108;119 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. The most common mutations were S72G, N93D and S192P, and, of these, N93D was the most relevant, given that all the samples with this mutation were associated with similar symptoms of pain and sensitivity. 2018 Virology journal Discussion HTLV1 S72G;N93D;S192P;N93D 31;37;46;68 35;41;51;72 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. The S192P mutation, while relatively frequent, could not be linked systematically to symptoms, given that two patients were asymptomatic. 2018 Virology journal Discussion HTLV1 S192P 4 9 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. Two of the six patients with HAM/TSP presented amino acid mutations, one with S72G and the other with L70I and S103P. 2018 Virology journal Discussion HTLV1 S72G;L70I;S103P 78;102;111 82;106;116 HTLV-1-associated myelopathy/tropical spastic paraparesis 29 36 29716616 Stability of the HTLV-1 glycoprotein 46 (gp46) gene in an endemic region of the Brazilian Amazon and the presence of a significant mutation (N93D) in symptomatic patients. While it was also among the most frequent mutations, S72G was also found in an individual with more than one amino acid mutation in the sequence of the gp46 gene. 2018 Virology journal Discussion HTLV1 S72G 53 57 gp46 152 156