Morphological alterations in minor salivary glands of HTLV1+ patients: A pilot study

BACKGROUND: Among the complex of HTLV­associated 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 HTLV­1, in minor salivary glands of patients with dryness symptoms. METHODS: We have assessed HTLV­1­seropositive patients (HTLV­1 group) and patients with SS (SS group). We used formalin­fixed, paraffin­embedded minor salivary gland tissue to evaluate the morphological aspects and, by means of immunohistochemistry, the presence of Tax protein, CD4, CD8 and CD20 cells. Additionally, viral particles and proviral load were analysed by PCR. RESULTS: The HTLV­1 group had the highest prevalence of non­specific chronic sialadenitis (85.71%; P = 0.017) and greater amount of T CD8+ cells. In the SS group, focal lymphocytic sialadenitis (80%; P = 0.017) prevailed, with a greater amount of B CD20+. 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 HTLV­1­seropositive patients have different patterns of morphological/inflammatory alterations, suggesting a likely difference in the process of immune activation

In vitro basal T-cell proliferation among asymptomatic Human T cell Leukemia Virus type 1 patients co-infected with hepatitis C and/or Human Immunodeficiency Virus type 1.

BACKGROUND: 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. OBJECTIVE: 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. MATERIAL AND METHODS: 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. RESULTS: 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. CONCLUSION: 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.

In vitro basal T-cell proliferation among asymptomatic Human T cell Leukemia Virus type 1 patients co-infected with hepatitis C and/or Human Immunodeficiency Virus type 1

ABSTRACT Background: 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. Objective: 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. Material and methods: 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. Results: 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. Conclusion: 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.

Meningococcal meningitis: clinical and laboratorial characteristics, fatality rate and variables associated with in-hospital mortality.

Meningococcal meningitis is a public health problem. The aim of this study was to describe the clinical characteristics of patients with meningococcal meningitis, and to identify associated factors with mortality. This was a retrospective study, between 2006 and 2011, at a referral center in São Paulo, Brazil. Logistic regression analysis was used to identify factors associated with mortality. We included 316 patients. The median age was 16 years (IQR: 7-27) and 60% were male. The clinical triad: fever, headache and neck stiffness was observed in 89% of the patients. The cerebrospinal triad: pleocytosis, elevated protein levels and low glucose levels was present in 79% of patients. Factors associated with mortality in the multivariate model were age above 50 years, seizures, tachycardia, hypotension and neck stiffness. The classic clinical and laboratory triads of meningococcal meningitis were variable. The fatality rate was low. Age, seizures and shock signs were independently associated with mortality.

Meningococcal meningitis: clinical and laboratorial characteristics, fatality rate and variables associated with in-hospital mortality / Meningite meningocócica: características clínicas e laboratoriais, taxa de letalidade e variáveis associadas com mortalidade intra-hospitalar

ABSTRACT Meningococcal meningitis is a public health problem. The aim of this study was to describe the clinical characteristics of patients with meningococcal meningitis, and to identify associated factors with mortality. This was a retrospective study, between 2006 and 2011, at a referral center in São Paulo, Brazil. Logistic regression analysis was used to identify factors associated with mortality. We included 316 patients. The median age was 16 years (IQR: 7–27) and 60% were male. The clinical triad: fever, headache and neck stiffness was observed in 89% of the patients. The cerebrospinal triad: pleocytosis, elevated protein levels and low glucose levels was present in 79% of patients. Factors associated with mortality in the multivariate model were age above 50 years, seizures, tachycardia, hypotension and neck stiffness. The classic clinical and laboratory triads of meningococcal meningitis were variable. The fatality rate was low. Age, seizures and shock signs were independently associated with mortality.

RESUMO Meningite meningocócica (MM) é um problema de saúde pública. Os objetivos deste estudo foram descrever características clinicas de pacientes com MM, e identificar fatores associados à mortalidade intra-hospitalar. Trata-se de um estudo retrospectivo, entre 2006 e 2011, em um centro de referência, São Paulo, Brasil. Análise de regressão logística multivariada foi usada para identificar fatores associados na admissão com mortalidade intra-hospitalar. Foram incluídos 316 casos. A média de idade foi 16 anos (IQR: 7–27) e 189 (60%) eram do sexo masculino. A tríade clínica: febre, cefaléia e rigidez de nuca foi observada em 89% dos casos. A tríade do exame de líquor: pleocitose, proteinorraquia elevada e hipoglicorraquia ocorreu em 79% dos casos. Fatores associados à mortalidade no modelo multivariado foram: idade acima de 50 anos, convulsões, taquicardia, hipotensão e rigidez de nuca. Tríades clínicas e laboratoriais clássicas de MM foram variáveis. Na admissão, idade, convulsões, taquicardia e hipotensão associaram-se independentemente com o desfecho.