Isolation of extended-spectrum beta-lactamases producing strains on effluent of state hospital from Boa Vista-RR

The extended spectrum beta-lactamase (ESBL) producing bacteria are widespread in hospital environments. The incorrect disposal of clinical waste in hospital effluents, allows them to present high concentrations of bacteria with antimicrobial resistance profiles that present an environmental risk to the extent that they allow the dissemination. This research covers the characterization of the presence of multi-resistant antimicrobial bacteria in strains isolated from hospital effluents, whose associated risks include the spread of pathogenic microorganisms in the environment. To complete this research, the proposed objectives were: characterization of the hospital effluent strains generated by the General Hospital of Roraima (GHR) and research of the resistance genes responsible for ESBL coding and hydrolysis to the antimicrobials of the class of cephalosporins, penicillins and monobactams. Samples were collected from the hospital septic tank from June 2014 to June 2016, submitted to molecular identification for the detection of genes through the polymerase chain reaction (PCR). The results showed the presence of ESBL in all of the collected tanks and a multi-resistance profile. ESBL genes were identified on isolated frequencies and they were combined. The results indicated the widespread dissemination of the ESBL genes in the GHR effluent

Phylogenetic analysis and genotype distribution of Hepatitis B Virus (HBV) in Roraima, Brazil

Hepatitis B virus (HBV) infection is a serious global health problem. HBV has a high viral genetic diversity, with 10 genotypes recognized. In Brazil, the Roraima State is the third in the Northern region regarding the number of hepatitis B cases. On the other hand, few data on HBV genotyping and phylogenetic analysis are available. The purpose of this study is to characterize the HBV genotypes circulating in Roraima State. Of the 113 chronic hepatitis B patients enrolled in this study, 40 were HBV-DNA positive. A fragment of 280 bp (S gene) was amplified by PCR and submitted to nucleotide sequencing. A dataset containing the viral sequences obtained in this study, plus 130 obtained from GenBank was used for genotyping by phylogenetic analysis. The HBV subgenotype distribution found was A1 (62.5%), A2 (7.5%), D2, D3, D4 (2.5%), F2a (12.5%), and F3 (10%). We characterized the genotypes and subgenotypes of HBV circulating among patients in the State of Roraima. In addition, our study shows for the first time the HBV/F3 genotype circulating in Brazil. In conclusion, our findings showed a high diversity of HBV genotypes in Roraima, which is also found in other Brazilian geographical regions

Dengue Virus Serotype 4, Roraima State, Brazil

Universidade Federal de Roraima. Boa Vista, RO, Brazil.Laboratório Central de Roraima. Boa Vista, RO, Brazil.Universidade Federal de Roraima. Boa Vista, RO, Brazil.Universidade Federal de Roraima. Boa Vista, RO, Brazil.Universidade Federal de Roraima. Boa Vista, RO, Brazil.Universidade Federal de Roraima. Boa Vista, RO, Brazil.Universidade Federal de Roraima. Boa Vista, RO, Brazil.Instituto Nacional de Pesquisas da Amazônia. Manaus, AM, Brazil.Fundação Oswaldo Cruz. Instituto Leônidas e Maria Deane. Rio de Janeiro, RJ, Brazil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Ananindeua, PA, Brasil.Ministério da Saúde. Secretaria de Vigilância em Saúde. Instituto Evandro Chagas. Ananindeua, PA, Brasil

SARS-CoV-2 uses CD4 to infect T helper lymphocytes

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the agent of a major global outbreak of respiratory tract disease known as Coronavirus Disease 2019 (COVID-19). SARS-CoV-2 infects mainly lungs and may cause several immune-related complications, such as lymphocytopenia and cytokine storm, which are associated with the severity of the disease and predict mortality. The mechanism by which SARS-CoV-2 infection may result in immune system dysfunction is still not fully understood. Here, we show that SARS-CoV-2 infects human CD4+ T helper cells, but not CD8+ T cells, and is present in blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients. We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS-CoV-2 in T helper cells. This leads to impaired CD4 T cell function and may cause cell death. SARS-CoV-2-infected T helper cells express higher levels of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may contribute to a poor immune response in COVID-19 patients.</p

SARS-CoV-2 uses CD4 to infect T helper lymphocytes

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the agent of a major global outbreak of respiratory tract disease known as Coronavirus Disease 2019 (COVID-19). SARS-CoV-2 infects mainly lungs and may cause several immune-related complications, such as lymphocytopenia and cytokine storm, which are associated with the severity of the disease and predict mortality. The mechanism by which SARS-CoV-2 infection may result in immune system dysfunction is still not fully understood. Here, we show that SARS-CoV-2 infects human CD4+ T helper cells, but not CD8+ T cells, and is present in blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients. We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS-CoV-2 in T helper cells. This leads to impaired CD4 T cell function and may cause cell death. SARS-CoV-2-infected T helper cells express higher levels of IL-10, which is associated with viral persistence and disease severity. Thus, CD4-mediated SARS-CoV-2 infection of T helper cells may contribute to a poor immune response in COVID-19 patients.</p

FALSE-NEGATIVE DENGUE CASES IN RORAIMA, BRAZIL: AN APPROACH REGARDING THE HIGH NUMBER OF NEGATIVE RESULTS BY NS1 AG KITS

Serum samples from 150 NS1-negative (Platelia ELISA) patients presumptively diagnosed with dengue were analyzed by the TaqMan probed real-time reverse transcription PCR (TaqMan qRT-PCR) method. The qRT-PCR positive samples were tested for serotype by semi-nested RT-PCR and a qualitative immunochromatographic assay for IgG and IgM. Molecular detection methods showed 33 (22%) positive samples out of 150 NS1-antigen negative samples. Of these, 72% were collected up to day 2 after the onset of symptoms, when diagnostic sensitivity of NS1-antigen test assays is significantly enhanced. Most of the cases were not characterized as secondary infection. Twenty-eight samples were successfully serotyped, 75% of which for DENV-4, 14% for DENV-2, 7% for DENV-3 and 4% for DENV-1. These findings reaffirm the hyperendemic situation of the state of Roraima and suggest a lower sensitivity of the NS1 test, mainly when DENV-4 is the predominant serotype. Health care providers should therefore be aware of samples tested negative by NS1 antigen assays, especially when clinical symptoms and other laboratory data results show evidence of dengue infection

Evaluation of the potential use of GSTP1, GSTO1 and p53 genotype profiles as markers of thyroid cancer predisposition and response to treatment

Orientador: Laura Sterian WardTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias MedicasResumo: O desenvolvimento de métodos moleculares de rastreamento de indivíduos com risco de desenvolver câncer entre os portadores de nódulos na tiróide é uma questão urgente de Saúde Pública. O objetivo deste trabalho é analisar a utilidade do perfil genotípico de GSTP1, GSTO1 e p53 na identificação de risco para câncer de tiróide e na sua resposta terapêutica. Comparamos amostras de sangue periférico de 157 controles com 142 indivíduos com nódulos: 44 benignos (30 bócios e 14 adenomas foliculares- AF) e 98 malignos (77 carcinomas papilíferos- CP e 21 carcinomas foliculares- CF). Todos os pacientes foram tratados e seguidos de acordo com o mesmo protocolo. Os pacientes com câncer da tiróide apresentavam mais freqüentemente os polimorfismos de GSTP1 (câncer = 27.5% versus controle = 5.7% - p<0.0001) e os polimorfismos do códon 72 de p53 (câncer =12.2% versus controle =2% - p<0.001) do que na população controle. Não houve diferença entre pacientes e controles em relação ao perfil do gene GSTO. Estes genótipos variantes conferiram um aumento de risco para câncer de tiróide de mais de 7 vezes, tanto para GSTP1 (Odds ratio= 7.415; 95% CI: 2.472-22.243) como para o códon 72 de p53 (Odds ratio=7.023; 95% CI: 1.928-25.588). Os polimorfismos em GSTP1 e códon 72 p53 identificam câncer com sensibilidade de 75% e 80% e especificidade de 68% e 63%, respectivamente. Análise de regressão logística ajustada para sexo, idade e cor, mostra que estes polimorfismos de GSTP1 e p53, mas não os de GSTO1, são fatores independentes de risco para malignidade. Não houve correlação entre o perfil genotípico para qualquer gene e a resposta a terapia ou evolução dos pacientes com câncer. Sugerimos que o uso desses marcadores moleculares, combinado com as clássicas características clínico-epidemiológicas associadas à susceptibilidade ao câncer da tiróide, pode ser útil no rastreamento de malignidade entre os portadores de nódulos tiroidianos da população brasileiraAbstract: The development of screening tools designed to identify individuals at risk for thyroid odule cancer is of utmost necessity. The aim of the present research is to evaluate the utility of GSTP1, GSTO1 and p53 genotype profiles as markers of risk to thyroid cancer and its response to treatment. We compared peripheral blood samples from 157 controls to 144 patients with thyroid nodules: 44 benign (30 hyperplasias and 14 folicular adenomas - AF) and 98 malignant (77 papillary carcinomas - PC and 21 folicular carcinomas - FC). All patients were managed according to a standard protocol. Thyroid carcinoma patients presented more frequently GSTP1 (cancer = 27.5% versus controls = 5.7% - p<0.0001) and codon 72 of p53 (cancer =12.2% versus controls =2% - p<0.001) polymorphisms than the control population. There was no difference between cancer and controls regarding GSTO gene. These variant genotypes increased the risk for thyroid câncer more than 7 times for GSTP1 (Odds ratio= 7.415; 95% CI: 2.472-22.243) and codon 72 of p53 (Odds ratio=7.023; 95% CI: 1.928-25.588). GSTP1 and codon 72 p53 polymorphisms identify thyroid câncer with a sensitivity of 75% and 80% and specificity of 68% and 63%, respectively. Logistic regression analysis adjusted for gender, age and color demonstrated that GSTP1 and p53, but not GSTO1 polymorphisms are independent factors of risk for malignancy. There was no correlation between any genetic profile and the response to treatment or the outcome of cancer patients. Our data indicates that the use of these molecular markers, together with the classic clinico-epidemiologic features associated to thyroid cancer susceptibility may be useful in screening thyroid nodules malignancy in Brazilian populationDoutoradoClinica MedicaDoutor em Clínica Médic