ABSTRACT
This study defined the normal variation range for different subsets of T-lymphocyte cells count in two different Brazilian regions. We analysed the T-lymphocytes subpopulations (CD3+, CD4+, CD8+) in blood donors of two Brazilian cities, located in North (Belem, capital state of Para, indian background) and Northeast (Salvador, capital state od Bahia, African background) regions of Brazil. Results were compared according to gender, stress level (sleep time lower than 8 hours/day), smoking, and alcohol intake. Lymphocytes subpopulations were measured by flow cytometry. Five hundred twenty-six blood donors from two Brazilians cities participated in the study: 450 samples from Bahia and 76 samples from Pará. Most (60 percent) were men, 59 percent reported alcohol intake, 12 percent were smokers, and 80 percent slept at least 8 h/day. Donors from Bahia presented with significantly higher counts for all parameters, compared with Para. Women had higher lymphocytes levels, in both states, but only CD4+ cells count was significantly higher than men's values. Smokers had higher CD4+ counts, but sleep time had effect on lymphocytes levels only for Para's donors (higher CD3+ and CD4+ counts). That state had also, a higher proportion of donors reporting sleep time <8 h/day. The values for CD3, CD4 and CD8+ cells count were significantly higher in blood donors from Bahia than among those from Pará. Female gender, alcohol intake, stress level, and smoking were associated with higher lymphocyte counts. The use of a single reference range for normal lymphocytes count is not appropriate for a country with such diversity, like Brazil is.
Subject(s)
Female , Humans , Male , Alcohol Drinking/immunology , Blood Donors , Smoking/immunology , Stress, Psychological/immunology , T-Lymphocyte Subsets/cytology , Brazil , Flow Cytometry , Lymphocyte Count , Reference ValuesABSTRACT
The present study investigated the frequency of the mutations at positions -550 and -221 of the mannose-binding lectin (MBL) gene in a sample of 75 human T-cell lymphotropic virus (HTLV) infected patients and 96 HTLV seronegative controls, in order to evaluate the occurrence of a possible association between the polymorphism and HTLV infection. A sequence specific primer-polymerase chain reaction was used for discrimination of the polymorphism. The analysis of allele frequencies at position -550 did not show any significant differences between HTLV infected group and controls, but there was a significant difference at position -221. The comparative analysis of haplotypes frequencies were not significant, but the genotype frequencies between the two groups, revealed a higher prevalence of genotype LYLX (25.3 percent), associated with medium and low MBL serum levels among HTLV infected subjects. The odds ratio estimation demonstrated that the presence of genotype LYLX was associated with an increased risk of HTLV infection (p = 0.0096; 1.38 < IC95 percent < 7.7605). There was no association between proviral load and the promoter polymorphism, but when promoter and exon 1 mutations were matched, it was possible to identify a significant higher proviral load among HTLV infected individuals carrying haplotypes correlated to low serum levels of MBL. The present study shows that the polymorphism in the promoter region of the MBL gene may be a genetic marker associated with HTLV infection, and emphasizes the need for further studies to determinate if the present polymorphism have any impact on diseases linked to HTLV infection.
Subject(s)
Adult , Female , Humans , Male , HTLV-I Infections/virology , HTLV-II Infections/virology , Human T-lymphotropic virus 1/genetics , /genetics , Mannose-Binding Lectin/genetics , Polymorphism, Genetic/genetics , Case-Control Studies , Disease Susceptibility , Genetic Markers/genetics , Haplotypes , Mutation/genetics , Polymerase Chain ReactionABSTRACT
Os autores relatam um caso de leucemia linfoblástica aguda (ALL) que no exame citogenético de células da medula óssea apresentou manomalias cromossômicas já descritas nesta condiçäo del(6)(q23); t(9;22)(q34;q11), ao lado das alteraçöes cromossômicas del(4)(p14) + 4ace e t(4;15)(p14;pter) ainda näo relatadas em ALL. Discutem a hipótese destas alteraçöes influenciarem na origem da malignidade, na pobre resposta ao tratamento e mau prognóstico observado no paciente pela possível ativaçäo de oncogenes em consequência das anomalias observadas