Subject of this dissertation thesis is the readiness of selected Czech banks and one cooperative lending institution to implementation of BASEL III capital requirements. Analysis is concentrated to current state of BASEL II and BASEL III in field of liquidity. For a purpose of comparison the indicator of Liquidity Coverage Ratio required by BASEL III is calculated and, when necessary, theoretically modeled. Institutions are analyzed whether they are ready and what measures should be implemented to fulfill liquidity requirements including the impact of these measures to the market and market of financial instruments.

Submitted by admin tede (tede@pucgoias.edu.br) on 2018-06-19T18:06:59Z No. of bitstreams: 1 SAMARA SOCORRO SILVA PEREIRA.pdf: 764936 bytes, checksum: 434a8cd13e6701c05b6ea08edda95150 (MD5) / Made available in DSpace on 2018-06-19T18:06:59Z (GMT). No. of bitstreams: 1 SAMARA SOCORRO SILVA PEREIRA.pdf: 764936 bytes, checksum: 434a8cd13e6701c05b6ea08edda95150 (MD5) Previous issue date: 2018-03-14 / Copy Number Variation (CNV) has been associated with intelectual disability (ID) and this condition occur in approximately 2% of world population. Chromosomal Microarray Analysis (CMA) is being indicated as first-tier test for individuals with ID and has also helped to understand the mechanisms of CNV formation, classification of these rearrangements, type of recurrence, and its origin. The aim of this study was to infer the parental chromosome origin of de novo pathogenic CNV in patients with ID and their mechanisms of formation. Patients with clinical indications of ID were referred to Replicon Research Group/LaGene for G-band karyotyping. CMA approach was done for patients without numerical and/or structural rearrangements results in karyotype. After performing CMA and classification of CNVs, the parental origin of pathogenic CNVs was done using Mendelian error check based on SNPs markers available by ChAs software. In addition, the UCSC Genome Browser website was used to detect Low Copy Repeats (LCR) surrounding the CNVs to infer the mechanisms of their formation. In the period from 2013 to 2015 was performed G-band karyotyping in 290 patients with clinical indication of ID and a total of 193/290 (66.5%) were diagnosed by Karyotype. The group of patients who were not diagnosed using the karyotype, only 76/97 (78.3%) agreed to continue the investigation by CMA’s approach. After performing CMA, a total of 15 de novo pathogenic CNVs were observed, 10 CNV of loss and 5 CNV of gain, in 13/76 (17.1%) patients. The analysis of the parental origin showed 60% of CNVs are of maternal origin and 40% of paternal origin. It was not possible to detect the influence of parental age in the formation of CNVs. After analyzing the presence of surrounding LCRs, it was observed that 46.7% are recurrent CNVs and the mechanism of formation was Non- Allelic Homologous Recombination (NAHR), and 71.4% of these recurrent CNVs are of maternal origin. These data are in agreement with studies that affirm that the majority of CNVs of paternal origin are nonrecurrent due to germ cells replicate many times their genetic material in the pre-meiotic phase, being possible to infer the mechanism of formation of CNV that may have been by Microhomology-mediated break-induced replication (MMBIR) or Non-homologous end joining (NHEJ). / A variação no número de cópias (CNV) no genoma é um dos fatores etiológicos que pode desencadear a condição da deficiência intelectual (DI), sendo que esta condição atinge cerca de 2% da população mundial. A metodologia de análise cromossômica por microarranjo (CMA) além de ser indicada como teste de primeira escolha para pacientes com DI, tem ajudado também na compreensão da formação de CNVs e classificação destes rearranjos, quanto à patogenicidade, o tipo de recorrência e sua origem. E este estudo objetivou inferir a origem cromossômica parental das CNVs de novo patogênicas em pacientes com DI e seu mecanismo de formação. Os pacientes com indicação clínica de DI foram encaminhados ao Núcleo de Pesquisas Replicon/LaGene para realização do cariótipo com bandeamento GTG, e subsequentemente, os que não tiveram alteração numérica e/ou estrutural no cariótipo foram convidados a continuar a investigação em nível genômico, pela metodologia de CMA. Após realização do CMA e classificação das CNVs, foram realizadas a análise da origem parental das CNVs de novo patogênicas pela análise do erro mendeliano usando os marcadores de SNPs disponibilizado pelo software ChAS. Adicionalmente, foi usado o UCSC Genome Browser para detectar Repetições De Poucas Cópias (LCR) circundantes as CNVs para inferir o mecanismo de formação das mesmas. Foi realizado o cariótipo em 290 pacientes com indicação clínica de DI entre os anos de 2013 a 2015 e em 193/290 (66,5%) foram diagnosticados pelo cariótipo. Do conjunto de pacientes que não foram diagnosticados usando o cariótipo, apenas 76/97 (78,3%) aceitaram continuar a investigação pelo CMA. Após realizar o CMA, foi observado 15 CNVs de novo patogênicas, 10 CNVs de perda e 5 CNVs de ganho, em 13/76 (17,1%) pacientes. Na análise da origem parental, observou-se que 60% das CNVs são de origem materna e 40% de origem paterna. Não foi possível detectar a influência da idade parental na formação das CNVs. Ao analisar a presença de LCRs circundantes, observou-se que 46,7% das CNVs de novo patogênicas são recorrentes e o mecanismo de formação foi a Recombinação Homologa Não Alélica (NAHR), e 71,4% dessas CNVs recorrentes são de origem materna. Esses dados corroboram com os estudos que afirmam que a maioria das CNVs de origem paterna são não recorrentes devido às células germinativas replicarem inúmeras vezes o seu material genético na fase pré-meiótica, sendo possível inferir sobre o mecanismo de formação que pode ter sido por Replicação Induzida por Quebra e Mediada por Microhomologia (MMBIR) ou Junção de Extremidade Não Alélica (NHEJ).

Le génotypage d’une famille jordanienne consanguine constituée de 5 frères globozoospermiques et de 3 frères fertiles sur puce Affymetrix, a permis d’identifier un nouveau gène responsable de la globozoospermie situé dans un intervalle de 6.4Mb en 12q14.2. Au regard de son expression prédominante dans le testicule et l’implication de son orthologue, chez C. elegans, dans la polarisation cellulaire, le gène DPY19L2 est un gène candidat parfait. Le gène, codant pour une protéine transmembranaire, est flanqué par deux séquences répétées (LCRs) qui partagent 96,5% d’identité. Dans une première étude, une délétion de 200Kb englobant l’ensemble du gène a été mise en évidence chez les 4 frères infertiles de cette famille jordanienne ainsi que chez 3 autres patients non apparentés. Nous avons ensuite recruté une plus grande cohorte de 54 patients. Parmi ces patients, 20 sont homozygotes pour la délétion de DPY19L2 et 7 sont hétérozygotes composites associant la délétion hétérozygote et une mutation ponctuelle. En outre, nous avons identifié, 4 patients avec des mutations ponctuelles homozygotes. Par conséquent, la fréquence d’implication de DPY19L2 s’élève à 66.7%. En tout, 9 points de cassures, regroupés en deux hotspots au sein des LCRs, ont pu être mis en évidence. Ceci confirme que le mécanisme sous-jacent de la délétion est une recombinaison homologue non allélique (NAHR) entre les LCRs. En conclusion, nous confirmons que DPY19L2 est le principal gène de la globozoospermie et nous élargissons le spectre des mutations possible dans ce gène. / Performing a genome wide scan by SNP microarray on a Jordanian consanguineous family where five brothers were diagnosed with complete globozoospermia, we show in a first study that the four out of five analysed infertile brothers carried a homozygous deletion of 200 kb on chromosome 12 encompassing only DPY19L2. The gene encodes for a transmembrane protein and is surrounded by two low copy repeats (LCRs). Very similar deletions were found in three additional unrelated patients. Later, we have pursued our patient screen by recruiting a largest cohort of patients. Out of a total of 54 patients analysed, 36 (66.7%) showed a mutation in DPY19L2. Out of 36 mutated patients, 20 are homozygous deleted, 7 heterozygous composite and 4 showed a homozygous point mutation. We characterized a total of nine breakpoints that clustered in two recombination hotspots, both containing direct repeat elements. These findings confirm that the deletion is due to a nonallelic homologous recombination (NAHR) between the two LCRs. Thus, Globozoospermia can be considered as a new genomic disorder. This study confirms that DPY19L2 is the major gene responsible for globozoospermia and enlarges the spectrum of possible mutations in the gene.

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal.

Human Papillomavirus (HPV) is one of the most common causes of sexually transmitted disease worldwide. Infections by high-risk HPVs, such as HPV-18, have been associated etiologically with cervical cancer. The successful development of HPV vaccines may be beneficial to the HPV-na??ve population, but women that have already been exposed to the virus are still at risk of developing HPV-associated malignancies. A need for a systemic cure for HPV-infection therefore still exists. Gene therapies using tissue-specific promoters have been reported to be a promising tool for treating cancers; however, few studies have explored this possibility for cervical cancer. The aim of this project is to construct a gene expression vector that can specifically target HPV-infected cervical cancer cells, by making use of the activity and selectivity of the P105 promoter which is determined by transcription control elements within the HPV-18 long control region (LCR). The first part of this study involved the construction of LCR deletion plasmids, and examining the subsequent level of gene expression induced within different mammalian cell lines. The results suggest the LCR to be capable in achieving cervical cancer-specific gene expression. The 3′-end of the viral L1 gene upstream of the LCR appeared to have a repressive effect on the promoter and therefore should be excluded for maximum LCR promoter activity. The second part of the project involved site-directed mutagenesis studies performed on selected transcription factor binding sites with an attempt to further increase the level of LCR promoter activity and specificity towards HPV-infected cervical cancer cells. The results suggest that a GRE/YY1 mutation may significantly enhance promoter activity. In terms of promoter regulation, the E2BSs appeared to be responsible for promoter activation in the absence of viral E2 proteins. The findings of this study suggest a possible gene therapy approach towards the treatment of cervical cancer. By making use of the activity and specificity of the HPV-18 P105 promoter to induce cervical carcinoma-specific expression of appropriate therapeutic genes, suicidal phenotypes can be introduced selectively within HPV-positive cervical cancer cells while normal HPV-negative cells are unaffected.

Human Papillomavirus (HPV) is one of the most common causes of sexually transmitted disease worldwide. Infections by high-risk HPVs, such as HPV-18, have been associated etiologically with cervical cancer. The successful development of HPV vaccines may be beneficial to the HPV-na??ve population, but women that have already been exposed to the virus are still at risk of developing HPV-associated malignancies. A need for a systemic cure for HPV-infection therefore still exists. Gene therapies using tissue-specific promoters have been reported to be a promising tool for treating cancers; however, few studies have explored this possibility for cervical cancer. The aim of this project is to construct a gene expression vector that can specifically target HPV-infected cervical cancer cells, by making use of the activity and selectivity of the P105 promoter which is determined by transcription control elements within the HPV-18 long control region (LCR). The first part of this study involved the construction of LCR deletion plasmids, and examining the subsequent level of gene expression induced within different mammalian cell lines. The results suggest the LCR to be capable in achieving cervical cancer-specific gene expression. The 3′-end of the viral L1 gene upstream of the LCR appeared to have a repressive effect on the promoter and therefore should be excluded for maximum LCR promoter activity. The second part of the project involved site-directed mutagenesis studies performed on selected transcription factor binding sites with an attempt to further increase the level of LCR promoter activity and specificity towards HPV-infected cervical cancer cells. The results suggest that a GRE/YY1 mutation may significantly enhance promoter activity. In terms of promoter regulation, the E2BSs appeared to be responsible for promoter activation in the absence of viral E2 proteins. The findings of this study suggest a possible gene therapy approach towards the treatment of cervical cancer. By making use of the activity and specificity of the HPV-18 P105 promoter to induce cervical carcinoma-specific expression of appropriate therapeutic genes, suicidal phenotypes can be introduced selectively within HPV-positive cervical cancer cells while normal HPV-negative cells are unaffected.

No description available.

Submitted by Irene Nascimento (irene.kessia@ufpe.br) on 2016-06-28T18:01:45Z No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) AnaPavla_Tese.pdf: 2030041 bytes, checksum: d62d754a4e28b637ecec9ecbd30a1fb2 (MD5) / Made available in DSpace on 2016-06-28T18:01:45Z (GMT). No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) AnaPavla_Tese.pdf: 2030041 bytes, checksum: d62d754a4e28b637ecec9ecbd30a1fb2 (MD5) Previous issue date: 2015-02-25 / CAPES / Cerca de 265 mil mulheres morrem todos os anos vítimas de câncer cervical. Infecções persistentes causadas por Papilomavírus humano de alto risco oncogênico (HR HPVs) é uma condição necessária, porém não suficiente para o desenvolvimento de lesões cervicais e câncer cervical. Dessa forma, diversos fatores ambientais e genéticos estão envolvidos na carcinogênese cervical. Dentre os fatores genéticos, as variantes genéticas dos HR HPVs parecem estar relacionados com o risco de infecções persistentes e desenvolvimento de lesões e câncer cervical. Assim, o presente estudo investigou: 1) A variabilidade genética de um fragmento do gene L1 dos HPV16, 31, 53, 54, 56, 58, 61, 62, 66, 70 e 81 em amostras biológicas de pacientes oriundos dos Estados de Pernambuco, Alagoas e Sergipe, Nordeste do Brasil; 2) A variabilidade genética da LCR dos HR HPVs 16, 31 e 58 oriundas de pacientes dos Estados de Pernambuco, Alagoas e Sergipe, Nordeste do Brasil; 3) Uma possível associação entre os polimorfismos virais do gene L1 e o risco para desenvolver lesões cervicais nas pacientes do Nordeste do Brasil. Para tanto, a detecção do DNA viral foi realizada em amostras biológicas de 784 pacientes. Os fragmentos parciais do gene L1 e da LCR dos HPVs mencionados foram sequenciados. Análises in silico de possíveis epitopos de células B e de células T foram efetuadas nas regiões de mutação não-sinônima no gene L1. Além disso, análises in silico dos sítios de ligação dos fatores transcricionais foram realizadas em regiões de alteração nucleotídica da LCR. Foram detectados 23 tipos de HPVs: HPVs 6, 11, 16, 18, 31, 33, 35, 39, 45, 52, 53, 54, 56, 58, 61, 62, 66, 70, 72, 81, 82, 83 e 84. Com relação ao gene L1 dos HPV analisados, foram detectadas 98 mutações, sendo 96/98 substituições de bases, 1/98 deleção e 1/98 inserção de nucleotídeo. Dentre estas alterações nucleotídicas no gene L1, 29,6% são mutações não sinônimas. Ademais, 18,36% das variações detectadas no gene L1 estavam inseridas em epitopos de células B, 25,5% inseridos em regiões de MHC Classe I e 18,36% inseridos em regiões de MHC Classe II. Um total de 8,1% das variações genéticas observadas no gene L1 dos HPV estudados foram descritos pela primeira vez na literatura. Em relação a LCR, foram detectadas 95 mutações, sendo 88/95 substituições de bases, 5/98 deleções e 2/95 inserções de nucleotídeos. Um total de 51,5% das mutações detectadas estão inseridas em sítios de ligação dos fatores transcricional celular e/ou viral. Além disso, 3,1% das variações genéticas encontradas na LCR foram descritas pela primeira vez na literatura. As análises filogenéticas mostraram a presença das variantes A e D do HPV16, A e C do HPV31 e A, B, C e D do HPV58 circulante no Nordeste do Brasil. Com relação a repercussão biológica das mutações do gene L1 do HPV16, não foram observadas associações significativas (p>0.05) entre os polimorfismos do gene L1 e o risco para desenvolver lesões cervicais. Entretanto, a combinação de determinados alelos destes polimorfismos virais está fortemente associada com o risco de desenvolver lesão cervical. Assim, a detecção das principais variantes e de alterações nucleotídicas com potencial impacto biológico circulantes no Nordeste Brasileiro é importante face as diferenças na patogenicidade dos HPVs. / Approximately 265 thousand women die every year from cervical cancer. Persistent infections caused by high oncogenic risk Human papillomavirus (HR HPV) are necessary but not sufficient condition for the development of cervical lesions and cervical cancer. Therefore, several environmental and genetic factors are involved in cervical carcinogenesis. Concerning the genetic factors, variants of HR HPV seem to be related to the risk of persistent infections and the development of lesions and cervical cancer. In this sense, the present study aimed to investigate: 1) The genetic variability of a L1 gene fragment from HPV16, 31, 53, 54, 56, 58, 61, 62, 66, 70 and 81 in biological samples of patients from Pernambuco, Alagoas and Sergipe states, Northeastern Brazil; 2) The genetic variability of the LCR of HR HPVs 16, 31 and 58 of patients from from Pernambuco, Alagoas and Sergipe states, Northeastern Brazil; 3) Possible association between the viral polymorphisms of the L1 gene and the risk to develop cervical lesions in patients from the Brazilian Northeast. To achieve that, viral DNA detection was performed in biological samples from 784 patients. Partial fragments of the L1 gene and the LCR of the abovementioned HPVs were sequenced. In silico predictions of possible B cells and T cells epitopes were performed in regions of non-synonymous mutation of the L1 gene. Moreover, in silico predictions of the binding sites of transcriptional factors were performed in nucleotide change regions within LCR. Twenty-three HPV types were detected: HPVs 6, 11, 16, 18, 31, 33, 35, 39, 45, 52, 53, 54, 56, 58, 61, 62, 66, 70, 72, 81, 82, 83 e 84. Regarding the L1 gene from the analyzed HPVs, 98 mutations were detected, in which 96 are nucleotide substitutions, 1 is deletion and 1 is nucleotide insertion. Among these nucleotide changes in the L1 gene, 29.6% are non-synonymous mutations. Moreover, 18.36% of the nucleotide changes are located in B cell epitopes, 25.5% located in MHC Class I regions and 18.36% located in MHC Class II regions. Finally, 8.1% of the genetic variations in the L1 gene of the studied HPVs were observed for the first time. Concerning LCR, 95 mutations were detected, in which 88 are nucleotide substitutions, 5 are deletions and 2 are nucleotide insertions. A total of 51.5% of the detected mutations are located in binding sites of cellular and/or viral transcriptional factors. Additionally, 3.1% of the genetic variations found in LCR were described for the first time. Phylogenetic analisys showed the presence of A and D variants of the HPV16, A and C variants of the HPV31, and A, B, C and D variants of the HPV58 circulating in the Brazilian Northeast. In regard to the biological repercussion of the L1 gene mutations of the HPV16, no significant associations were observed (p>0.05) between L1 gene polymorphism and the risk to develop cervical lesions. However, the combination of certain alleles from these viral polymorphisms is firmly associated to the risk to develop cervical lesion. Thus, the detection of the main circulating variants with potential biological impact in the Brazilian Northeast is important in view of the differences in the pathogenicity of the HPV.

<p>Helminth exposure, allergy and asthma each induce cellular responses in lymphoid and peripheral tissues that give rise to type-2 inflammation. Essential molecular mediators of this response are type-2 cytokines interleukin(IL)-4 and IL-13 derived from various subsets of immune cells. In lymphoid tissues, CD4+ Tfh cells make IL-4 to elicit IgE and high-affinity IgG1 production. In peripheral sites of infection, group 2 innate lymphoid (ILC2) cells make IL-13 and Th2 cells make both IL-13 and IL-4. Together, these cells mediate smooth muscle contraction, mucus production and recruitment of other innate effector cells, all of which are hallmarks of type-2 inflammation. As central mediators of type-2 inflammation, understanding the cell-specific expression and molecular regulation of type-2 cytokines in CD4+ T cells and ILC2 cells may lead to new therapies that ameliorate allergic disease and helminth infections. </p><p>The AP-1 factor basic leucine zipper transcription factor ATF-like (BATF) has been identified as a pioneer factor in in vitro-generated Th17 cells. BATF facilitates chromatin remodeling at the IL-17 locus as well as loci of key Th17-associated lineage specifying factors. It has also been deemed essential to the generation of functional humoral immunity through the development of follicular helper T (Tfh) cells and germinal center B cells. However, the role of BATF in the development and function of other CD4+ T helper subsets and innate immune cells in vivo has remained unclear. I show here that mice deficient in BATF do not develop type-2 inflammation after exposure to the parasitic helminth Nippostongylus brasiliensis. Since type-2 cytokine expression by Th2 and ILC2 cells is essential for expedient helminth expulsion, I hypothesized that BATF likely has a role in the development and/or induction of cytokine expression in CD4+ Th2 cells and ILC2 cells. Consistent with this hypothesis, I found that BATF utilizes a novel mechanism to control Th2 cytokine expression in Th2 cells. Specifically, BATF promotes permissive epigenetic modifications to alter the chromatin landscape early during Th2 cell differentiation. In addition, my data show that BATF deficiency inhibits the activation of ILC2 cells, preventing ILC2-mediated helminth clearance. </p><p>In addition to uncovering BATF-mediated regulations of type-2 inflammation, my work has revealed new insight into the role of a second bZIP transcription factor, cMaf, during type-2 immunity. As mentioned above, helminth exposure elicits IL-4 production by both CD4+ Tfh and Th2 cells. Although type-2 cytokine transcription has been well characterized in Th2 cells, Tfh cell-mediated IL-4 production has yet to be fully defined. Importantly, I show that IL-4 production by Tfh cells is sustained upon deletion of classical IL-4 regulatory factors signal transducer and activator of transcription 6 (STAT6) and STAT5 and is not dependent on high GATA-3 expression. In sum, Tfh-driven IL-4 production is induced independent of classical pathways in Th2 cells. </p><p>Presently, the non-canonical transcription factors involved in IL-4 production by Tfh cells remain unclear. C-Maf works with BCL6, the master regulator of Tfh cells, to elicit Tfh formation. However, the precise role of c-Maf in Tfh cell fate and function remains unclear. So far, it has been shown that in Th2 cells, c-Maf binds to the IL-4 promoter and in Tfh cells, c-Maf binds to the CNS2 enhancer of the IL-4 locus to regulate IL-4 expression. Therefore, I hypothesized that c-Maf is important in non-canonical, GATA-3-independent IL-4 production by Tfh cells. </p><p>Here, I show that Tfh cells lacking canonical Th2 pathways for IL-4 expression express high levels of c-Maf and IL-4 transcript. Deletion of c-Maf in CD4+ T cells resulted in normal induction of BCL6 expression. Thus the initial stages of Tfh cell generation were induced. However, cMaf-deficient CD4+ T cells did not express important molecules associated with Tfh cell migration. Immunohistochemistry also confirmed that c-Maf deficiency inhibited CD4+ T cell migration from the paracortex into the B cell follicle. </p><p>These defects did not inhibit cMaf-deficient CD4+ T cells from making IL-4 transcript; however, IL-4 protein production was significantly impaired. Together, these results demonstrate that c-Maf is essential for Tfh cell-mediated immunity by promoting CD4+ T cell migration to the B cell follicles and the production of IL-4 protein in the germinal centers. </p><p>Collectively, the objective of my thesis research is to define the roles of the bZIP transcription factors BATF and c-Maf in type-2 inflammation. My data demonstrate that BATF is essential for the differentiation and function of Tfh, Th2, and ILC2 cells during helminth infection. Additionally, I have shown that c-Maf is required for Tfh function and CD4+ T cell migration to the B cell follicle. Thus, BATF and c-Maf are central to the development of humoral and peripheral type-2 inflammatory responses against helminth infection. Given the wide spectrum of disorders associated with type-2 inflammation, the identification of factors relevant to the development and function of Th2-, ILC2- and Tfh-driven allergic pathologies is broadly relevant. A comprehensive characterization of core factors like BATF and c-Maf provide new avenues in which to explore novel therapies to modulate type-2 inflammatory responses.</p> / Dissertation

O diagnóstico de neurosífilis é freqüentemente dependente dos resultados dos testes serológicos e alterações no líquido cefalorraquidiano, mas a confiabilidade desses resultados em pacientes com infecção pelo HIV-1 tem sido questionada especialmente em pacientes assintomáticos com sífilis latente. O estudo se propõe avaliar a presença de DNA do T. pallidum no LCR de pacientes assintomáticos infectados pelo HIV, com o diagnóstico de sífilis. Amostras de LCR foram coletadas de 12 pacientes infectados pelo HIV atendidos em um terciário localizado no sul do Brasil , durante o período de 2012 a 2013. A presença de DNA do T. pallidum foram analisadas nas amostras de LCR pelo método de PCR “seminested”. Dados demográficos dos pacientes, parâmetros bioquímicos, celularidade e VDRL do LCR e linfócitos T-CD4 também foram analisados. Nas amostras de LCR de cinco dos 12 pacientes (40%) foram detectados o DNA do T. pallidum . Inesperadamente, nestes doentes, os níveis de contagem de células, proteína e glicose no LCR foram normais. Além disso , nenhuma destas cinco amostras de CSF apresentou uma reacção positiva VDRL. Os títulos de VDRL no soro foram semelhantes entre pacientes positivos e negativos para a presença T. pallidum DNA no LCR. A maioria dos pacientes com DNA de T. pallidum detectável apresentaram baixos títulos de VDRL no soro. O VDRL sérico elevado com título de 1:64 foi observada em apenas um paciente. Nossos resultados demostraram que os pacientes assintomáticos infectados pelo HIV com evidência de sífilis latente e LCR normais podem apresentar DNA de T. pallidum detectável no LCR. A detecção do DNA do T. pallidum pelo nosso seminested PCR pode fornecer informações adicionais além da análise convencional do LCR para o diagnóstico de neurossífilis. presença do DNA de T. pallidum no LCR em pacientes infectados pelo HIV com sífilis latente e resultados de LCR normais pode determinar uma mudança terapêutica do uso de penicilana benzatina intramuscular para o de penicilina cristalina intravenosa aquosa para o tratamento da sífilis. / Neurosyphilis diagnosis is frequently dependent upon the results of serological tests and cerebrospinal fluid abnormalities, but the reliability of findings in patients with HIV-1 infection has been questioned, especially asymptomatic patients with latent syphilis, We present the data on the presence of T. pallidum DNA in CSF from asymptomatic HIV-infected patients with the diagnosis of syphilis. CSF and serum samples were collected from 12 HIV-infected patients attending a tertiary care located in southern Brazil, during the period 2012 to 2013. In CSF samples from five of 12 patients (40%), we detected T. pallidum DNA. Unexpectedly, in these patients, CSF cell count, protein and glucose levels were normal. In addition, none of these 5 CSF samples presented a positive VDRL reaction. Serum VDRL titers were similar between patients with positive and negative CSF T. pallidum DNA. Most patients with detectable T. pallidum DNA presented low serum VDRL titers. Serum VDRL titer of 1:64 was observed in one patient. Our results have shown that asymptomatic HIV-infected patients with evidence of latent syphilis and normal CSF might present detectable T. pallidum DNA in the CSF. The detection of T. pallidum DNA by our seminested PCR provide additional information beyond conventional CSF analysis for diagnosis of neurosyphilis. The detection of T. pallidum DNA in the CSF despite normal CSF findings in HIV-infected patients could also provide a different therapeutic approach including the use of intravenous aqueous crystalline penicillin.