Background:The aim of this study was to evaluate the frequency, spectrum, in-hospital mortality rate, and factors associated with death in people living with HIV/AIDS (PLWHA) presenting with neurological diseases from a middle-income country, as well as estimate its one-year global death rate.Methods:This prospective observational cohort study was conducted at a Brazilian tertiary health center between January and July 2017. HIV-infected patients above 18 years of age who were admitted due to neurological complaints were consecutively included. A standardized neurological examination and patient and/or medical assistant interviews were performed weekly until the patient's discharge or death. The diagnostic and therapeutic management of the included cases followed institutional routines.Results:A total of 105 (13.2%) patients were included among the 791 hospitalized PLWHA. The median age was 42.8 [34-51] years, and 61% were men. The median CD4+ lymphocyte cell count was 70 (27-160) cells/mm3, and 90% of patients were experienced in combined antiretroviral therapy. The main diseases were cerebral toxoplasmosis (36%), cryptococcal meningitis (14%), and tuberculous meningitis (8%). Cytomegalovirus causing encephalitis, polyradiculopathy, and/or retinitis was the third most frequent pathogen (12%). Moreover, concomitant neurological infections occurred in 14% of the patients, and immune reconstitution inflammatory syndrome-related diseases occurred in 6% of them. In-hospital mortality rate was 12%, and multivariate analysis showed that altered level of consciousness (P = 0.04; OR: 22.7, CI 95%: 2.6-195.1) and intensive care unit (ICU) admission (P = 0.014; OR: 6.2, CI 95%: 1.4-26.7) were associated with death. The one-year global mortality rate was 31%.Conclusion:In this study, opportunistic neurological diseases were predominant. Cytomegalovirus was a frequent etiological agent, and neurological concomitant diseases were common. ICU admission and altered levels of consciousness were associated with death. Although in-hospital mortality was relatively low, the one-year global death rate was higher.
In the present pilot study, massively parallel sequencing (MPS) technology was used to investigate cellular small RNA (sRNA) levels in the peripheral blood mononuclear cells (PBMCs) of human T-lymphotropic virus type I (HTLV-I) infected asymptomatic carriers with monoclonal (ASM) and polyclonal (ASP) T cell receptor (TCR) γ gene. Blood samples from 15 HTLV-I asymptomatic carriers (seven ASM and eight ASP) were tested for the clonal TCR-γ gene and submitted for sRNA library construction together with blood samples of five healthy controls (HCs) using Illumina sequencing platform. The sRNA-sequencing reads were aligned, annotated and profiled using various bioinformatics tools. Based on these results, possible markers were validated in the study samples by performing reverse transcription-quantitative (RT-q)PCR analysis. A total of 76 known sRNAs and 52 putative novel sRNAs were identified. Among them, 44 known and 34 potential novel sRNAs were differentially expressed in the ASM and ASP libraries compared with HCs. In addition, 10 known sRNAs were exclusively dysregulated in the ASM group and one (transfer RNA 65) was significantly upregulated in the ASP group. Homo sapiens (hsa) microRNA (miRNA/mir)-23a-3p, -28-5p, hsa-let-7e-5p and hsa-mir-28-3p and -361-5p were the most abundantly upregulated mature miRNAs and hsa-mir-363-3p, -532-5p, -106a-5p, -25-3p and -30e-5p were significantly downregulated miRNAs (P<0.05) with a >2-fold difference between the ASM and ASP groups compared with HCs. Based on these results, hsa-mir-23a-3p and -363-3p were selected for additional validation. However, the quantification of these two miRNAs using RT-qPCR did not provide any significant differences. While the present study failed to identify predictive sRNA markers to distinguish between ASM and ASP, the MPS results revealed differential sRNA expression profiles in the PBMCs of HTLV-1 asymptomatic carriers (ASM and ASP) compared with HCs.
This study proposes to investigate the vertical and sexual HTLV-1 transmission rate in a coorte followed up in Sao Paulo, Brazil. The latter 173 HTLV-1-infected patients were selected until july 2014 (27.2% of 636 HTLV-1-infected individuals). Data were recorded using RedCap (Research Electronic Data Capture), transported to SPSS – Statistical Package for Social Sciences (v 20) and subjected to statistical analysis. To compare results between groups, one-way analysis of variance (one-way ANOVA test) was used. The vertical transmission rate found among 73 individuals born to HTLV-1-positive mothers was 6.8%. HTLV-1 concordant couples were compared to HTLV-1 discordant couples. Those coinfected with HIV were excluded from the sample. Among 91 individuals with stable partnership and without HIV, 49% did not know about the current partner serology: 39% of wives and 54.5% of husbands have not been tested. The horizontal transmission rate of HTLV-1 among those tested couples was 55.3%. Among men 68.2% of its wives were seropositive for HTLV-1, while among women 44.0% of its husbands were seropositive. HTLV-1 concordant couples (cases, n=6) were also compared to HTLV-1 discordant couples (controls, n=14), with respect to HTLV-1 proviral load. Those without HTLV-1 proviral load were excluded. In turn, the control group was subdivided into two subgroups: discordant couples with male index partner (n=5) and discordant couples with female index partner (n=9). Because of the impossibility of defining whether sexual transmission had occurred from man to woman or woman to man, for group 1 (concordant couples) we chose to use the average of the proviral loads of both partners in this group. Serodiscordant couples showed higher mean proviral loads (670 ±515 copias/104 peripheral blood mononuclear cell (PBMC)) compared with serodiscordant couples (282 ± 293 copias/104 PBMC) (p=0.045), probably associated with increased genital shedding of this virus and resulting increased risk of sexual transmission.
Background: Central nervous system involvement associated with Coronavirus Disease 2019 (COVID-19) has been reported, including cognitive impairment, even in patients with mild COVID-19. processes. Objective: To assess cognitive decline related to the SARS-CoV-2 infection in patients with neurological disease after COVID-19. Methods: Longitudinal prospective study developed to compare the cognitive performance of patients after COVID-19 based on cognitive complaints. The Addenbrooke´s Cognitive ExaminationRevised (ACE-R), a 100-point test, was applied for investigation, with cut-off score for cognitively normal individuals ≥ 78. Results: Fifty patients were evaluated, 33 women (66%). Thirty-six patients with cognitive complaint (72%), this being the only symptom in 18 (50%), more frequent in women (5:1). Among all patients, the mean score of ACE-R was 80.8 (SD 11) and median of 84. In patients with cognitive complaints, mean of 80.37 (SD 12.2) and median of 84. For the other patients, mean of 81.86 (SD 7.65) and median of 82.5 (p value = 0.9869). Cognitive decline was confirmed in 10/35 (28.57%) of patients with cognitive complaint, and in 4/14 (28.57%) of other patients (exacto de Fisher = 0.8809). Regarding the ACE-R subanalyses, impaired attention and orientation were observed in both groups. Conclusion: Cognitive complaint was not a predictor of cognitive decline, but impairment in attention and orientation were observed in the entire sample.
Background Among the complex of HTLV ‐associated diseases, Sjögren's syndrome ( SS ) is one of the most controversial. This work aims to detect morphological and inflammatory alterations, including clues of the presence of HTLV ‐1, in minor salivary glands of patients with dryness symptoms. Methods We have assessed HTLV ‐1‐seropositive patients ( HTLV ‐1 group) and patients with SS ( SS group). We used formalin‐fixed, paraffin‐embedded minor salivary gland tissue to evaluate the morphological aspects and, by means of immunohistochemistry, the presence of Tax protein, CD 4, CD 8 and CD 20 cells. Additionally, viral particles and proviral load were analysed by PCR . Results The HTLV ‐1 group had the highest prevalence of non‐specific chronic sialadenitis (85.71%; P = 0.017) and greater amount of T CD 8 + cells. In the SS group, focal lymphocytic sialadenitis (80%; P = 0.017) prevailed, with a greater amount of B CD 20 + . Both immunohistochemistry and PCR identified the Tax protein and its gene in the salivary glands of both groups and in similar proportions. Conclusion The results indicate that HTLV ‐1‐seropositive patients have different patterns of morphological/inflammatory alterations, suggesting a likely difference in the process of immune activation.
Infection with Human T cell Leukemia Virus type 1 can be associated with myelopathy/tropical spastic paraparesis (HAM/TSP) and other inflammatory diseases. Lymphocytes from about half of Human T cell Leukemia Virus type 1-infected subjects spontaneously proliferate in vitro, and how this phenomenon relates to symptomatic disease and viral burden is poorly understood.To evaluate T-cell proliferation in vitro among patients co-infected with Human T cell Leukemia Virus type 1/Hepatitis C Virus/Human Immunodeficiency Virus type 1.From 610 Human T cell Leukemia Virus-infected patients of the Human T cell Leukemia Virus outpatient clinic from Institute of Infectious Diseases "Emilio Ribas" in São Paulo, 273 agreed to participate: 72 had HAM/TSP (excluded from this analysis) and 201 were asymptomatic, a classification performed during a regular neurological appointment. We selected the subgroup made up only by the 201 asymptomatic subjects to avoid bias by the clinical status as a confounder effect, who had laboratory results of Human T cell Leukemia Virus type 1 proviral load and T-cell proliferation assay in our database. They were further grouped according to their serological status in four categories: 121 Human T cell Leukemia Virus type 1 asymptomatic mono-infected carriers; 32 Human T cell Leukemia Virus type 1/Hepatitis C Virus, 29 Human T cell Leukemia Virus type 1/Human Immunodeficiency Virus type 1, and 19 Human T cell Leukemia Virus type 1/Human Immunodeficiency Virus type 1/Hepatitis C Virus co-infected patients. Clinical data were obtained from medical records and interviews. DNA Human T cell Leukemia Virus type 1 proviral load (PVL) and T-cell proliferation (LPA) assay were performed for all samples.From a total of 273 subjects with Human T cell Leukemia Virus type 1, 80 presented co-infections: 29 had Human Immunodeficiency Virus type 1, 32 had Hepatitis C Virus, and 19 had Human Immunodeficiency Virus type 1 and Hepatitis C Virus. Comparing the groups based on their serological status, independently of being asymptomatic carriers, we observed a significant increase of PVL (p<0.001) and LPA (p=0.001). However, when groups were stratified according to their clinical and serological status, there was no significant increase in Human T cell Leukemia Virus type 1 PVL and LPA.No significant increase of basal T-cell proliferation among Human T cell Leukemia Virus type 1 co-infected was observed. This interaction may be implicated in liver damage, worsening the prognosis of co-infected patients or, on the contrary, inducing a higher spontaneous clearance of Hepatitis C Virus infection in Human T cell Leukemia Virus type 1 co-infected patients.
To provide an evidence-based approach to the use of therapies that are prescribed to improve the natural history of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP)-a rare disease.All 41 articles on the clinical outcome of disease-modifying therapy for HAM/TSP were included in a systematic review by members of the International Retrovirology Association; we report here the consensus assessment and recommendations. The quality of available evidence is low, based for the most part on observational studies, with only 1 double-masked placebo-controlled randomized trial.There is evidence to support the use of both high-dose pulsed methyl prednisolone for induction and low-dose (5 mg) oral prednisolone as maintenance therapy for progressive disease. There is no evidence to support the use of antiretroviral therapy. There is insufficient evidence to support the use of interferon-α as a first-line therapy.
Background HTLV-1 infection may is present among HCV or HIVinfected subjects and is associated with higher risk for HAM/TSP and other inflammatory diseases. Lymphocytes from about half of HTLV-1-infected subjects spontaneously proliferate in vitro, and how this phenomenon relates to symptomatic disease outcome and viral burden is poorly understood. Objective: Evaluate T-cell proliferation in vitro and HTLV-1 proviral load (PVL) among co-infected subjects.
Background:The aim of this study was to evaluate the frequency, spectrum, in-hospital mortality rate, and factors associated with death in people living with HIV/AIDS (PLWHA) presenting with neurological diseases from a middle-income country, as well as estimate its one-year global death rate.Methods:This prospective observational cohort study was conducted at a Brazilian tertiary health center between January and July 2017. HIV-infected patients above 18 years of age who were admitted due to neurological complaints were consecutively included. A standardized neurological examination and patient and/or medical assistant interviews were performed weekly until the patient's discharge or death. The diagnostic and therapeutic management of the included cases followed institutional routines.Results:A total of 105 (13.2%) patients were included among the 791 hospitalized PLWHA. The median age was 42.8 [34-51] years, and 61% were men. The median CD4+ lymphocyte cell count was 70 (27-160) cells/mm3, and 90% of patients were experienced in combined antiretroviral therapy. The main diseases were cerebral toxoplasmosis (36%), cryptococcal meningitis (14%), and tuberculous meningitis (8%). Cytomegalovirus causing encephalitis, polyradiculopathy, and/or retinitis was the third most frequent pathogen (12%). Moreover, concomitant neurological infections occurred in 14% of the patients, and immune reconstitution inflammatory syndrome-related diseases occurred in 6% of them. In-hospital mortality rate was 12%, and multivariate analysis showed that altered level of consciousness (P = 0.04; OR: 22.7, CI 95%: 2.6-195.1) and intensive care unit (ICU) admission (P = 0.014; OR: 6.2, CI 95%: 1.4-26.7) were associated with death. The one-year global mortality rate was 31%.Conclusion:In this study, opportunistic neurological diseases were predominant. Cytomegalovirus was a frequent etiological agent, and neurological concomitant diseases were common. ICU admission and altered levels of consciousness were associated with death. Although in-hospital mortality was relatively low, the one-year global death rate was higher.
Human T-Cell Lymphotropic Virus/Human Immunodeficiency Virus, and Hepatitis C Virus Coinfection: Clinical Outcomes After 22 Years of Follow-up in São Paulo City Jorge Casseb, Jorge Casseb Faculdade de Medicina da Universidade de São Paulo/Tropical Medicine Institute of São Paulo, São Paulo, BrazilLaboratory of Dermatology and Immunodeficiencies, Department of Dermatology, University of São Paulo Medical School, São Paulo, BrazilHuman Immunodeficiency Virus Outpatient Clinic–Secondary Immunodeficiencies Service (ADEE3002), Department of Dermatology of Hospital das Clínicas, University of São Paulo Medical School, Av. Dr. Enéas de Carvalho Aguiar, São Paulo, Brazil Correspondence: J. Casseb, Laboratory of Investigation in Dermatology and Immunodeficiencies, LIM56, Av. Dr. Enéas de Carvalho Aguiar 500, 3rd Floor, Building II, São Paulo, SP, Brazil (jcasseb@usp.br or alternative: rdcassia@uol.com.br). https://orcid.org/0000-0002-4553-2559 Search for other works by this author on: Oxford Academic PubMed Google Scholar Rosa Maria N Marcusso, Rosa Maria N Marcusso Institute of Infectious Diseases “Emilio Ribas” of São Paulo, São Paulo, Brazil Search for other works by this author on: Oxford Academic PubMed Google Scholar Mariana Monteiro, Mariana Monteiro Human Immunodeficiency Virus Outpatient Clinic–Secondary Immunodeficiencies Service (ADEE3002), Department of Dermatology of Hospital das Clínicas, University of São Paulo Medical School, Av. Dr. Enéas de Carvalho Aguiar, São Paulo, Brazil Search for other works by this author on: Oxford Academic PubMed Google Scholar Tatiane Assone, Tatiane Assone Faculdade de Medicina da Universidade de São Paulo/Tropical Medicine Institute of São Paulo, São Paulo, BrazilLaboratory of Dermatology and Immunodeficiencies, Department of Dermatology, University of São Paulo Medical School, São Paulo, Brazil Search for other works by this author on: Oxford Academic PubMed Google Scholar Michel E Y Haziot, Michel E Y Haziot Institute of Infectious Diseases “Emilio Ribas” of São Paulo, São Paulo, Brazil Search for other works by this author on: Oxford Academic PubMed Google Scholar Mario Peribanez-Gonzalez, Mario Peribanez-Gonzalez Institute of Infectious Diseases “Emilio Ribas” of São Paulo, São Paulo, Brazil Search for other works by this author on: Oxford Academic PubMed Google Scholar Luiz Augusto M Fonseca, Luiz Augusto M Fonseca Faculdade de Medicina da Universidade de São Paulo/Tropical Medicine Institute of São Paulo, São Paulo, BrazilLaboratory of Dermatology and Immunodeficiencies, Department of Dermatology, University of São Paulo Medical School, São Paulo, Brazil Search for other works by this author on: Oxford Academic PubMed Google Scholar Jerusa Smid, Jerusa Smid Institute of Infectious Diseases “Emilio Ribas” of São Paulo, São Paulo, Brazil Search for other works by this author on: Oxford Academic PubMed Google Scholar João V Luisi de Moura, João V Luisi de Moura Institute of Infectious Diseases “Emilio Ribas” of São Paulo, São Paulo, Brazil Search for other works by this author on: Oxford Academic PubMed Google Scholar Flávia E Dahy, Flávia E Dahy Institute of Infectious Diseases “Emilio Ribas” of São Paulo, São Paulo, Brazil Search for other works by this author on: Oxford Academic PubMed Google Scholar ... Show more Augusto Penalva de Oliveira Human Immunodeficiency Virus Outpatient Clinic–Secondary Immunodeficiencies Service (ADEE3002) Augusto Penalva de Oliveira Institute of Infectious Diseases “Emilio Ribas” of São Paulo, São Paulo, Brazil Search for other works by this author on: Oxford Academic PubMed Google Scholar Clinical Infectious Diseases, Volume 72, Issue 10, 15 May 2021, Pages 1865–1866, https://doi.org/10.1093/cid/ciaa1008 Published: 02 March 2021 Article history Received: 16 June 2020 Editorial decision: 19 June 2020 Accepted: 26 February 2021 Corrected and typeset: 02 March 2021 Published: 02 March 2021
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