Exposure source prevalence is associated with gender in hepatitis C virus patients from Rio de Janeiro, Brazil

BACKGROUND Hepatitis C virus (HCV) infection is a worldwide public health problem. A characterisation of the differences in exposure sources among genders will enable improvements in surveillance actions. METHODS Exposure data were obtained for 1180 confirmed HCV cases Brazil's mandatory reporting to epidemiological surveillance, which was directed by a reference laboratory in Rio de Janeiro, Brazil. The Chi-square test (χ2) was used to assess the associations between exposure sources and gender. The prevalence ratio (PR) was calculated for exposures that showed an association. RESULTS The results showed 57.7% cases were female, and associations with snorting drugs, sexual activity, surgery, aesthetic procedures, blood transfusions, and educational level were observed (p < 0.001). Men showed 2.53 (1.33-3.57), 4.83 (3.54-6.59), and 2.18 (1.33-3.57) times more exposure to sniffing drugs, risky sex and higher levels of education, respectively, than women. Women demonstrated 4.46 (3.21-6.21), 1.94 (1.43-2.63), and 3.10 (2.09-4.61) times more exposure to surgery, aesthetic procedures, and blood transfusions, respectively, than men. CONCLUSION Our results showed differences in risk behaviours associated with gender among HCV carriers. These data are likely to significantly influence clinical practice regarding the adoption of specific approaches for counselling and control policies to prevent the emergence of new cases and break the chain of transmission of the virus.

Caracterização da via dos Interferons e a via da proteína p53 em linhagens de células tumorais expostas ao dano genotóxico

O gene gbp-2 codifica uma proteína com função biológica pouco estudada, é altamente expresso após a indução de IFNγ e requer o fator de transcrição IRF-1 para sua indução. A regulação positiva de gbp-2 dependente da ativação da proteína supressora de tumor p53 foi recentemente descrita em uma linhagem de carcinoma de esôfago que expressa uma proteína mutante p53 termo-sensível. A ativação da proteína p53 por sinais de estresse, como dano ao DNA, induz genes que participam da parada do ciclo celular e apoptose. Nesse contexto, os principais objetivos dessa tese foram: (i) verificar a indução de gbp-2 após a ativação de p53 pelo dano genotóxico; (ii) correlacionar sua eventual indução com a ativação de IRF-1; (iii) correlacionar a indução de gbp-2 e de sua proteína com as respostas celulares após o dano ao DNA. Nessa tese, pela primeira vez foi demonstrado que o gene gbp-2 é induzido pelo dano genotóxico; essa indução correlacionou-se com a presença da proteína p53 selvagem em linhagens tumorais; o aumento de expressão de IRF-1 não foi suficiente para a indução de gbp-2 após o dano ao DNA; nas linhagens celulares nas quais houve a indução de gbp-2 a resposta predominante foi a de parada do ciclo celular. O estudo da relação entre a via dos IFNs e da p53 pode trazer importantes implicações do papel dos IFNs durante a carcinogênese.

The gene gbp-2 codes for a protein with an unknown biological function. Gbp-2 is highly expressed after the induction by IFNγ and requires the transcription factor IRF-1. Recently, the positive p53-dependent regulation of gbp-2 was described in an esophageal cell line, wich expresses a temperature-sensitive mutant p53. The activation of p53 by stress signal such as DNA damage is known to induce genes involved in cell cycle arrest and apoptosis. Within this context, the main objectives of this study were: (i) to evaluate gbp-2 induction upon p53 activation by genotoxic damage; (ii) to establish a correlation of an eventual gbp-2 induction with IRF-1 activation; (iii) to correlate gbp-2 induction with cellular response to DNA damage. In this study, it was demonstrated for the first time that gbp-2 may be induced by genotoxic effect and also that the induction occurred in p53wt cell lines. Furthermore it was demonstrated that an increase in the expression of IRF-1 was not sufficient to induce gbp-2 following DNA damage. In addition, within the cell lines at which a gbp-2 induction was observed the preferential response was arrest of cell cycle progression. The study of the correlation between IFN and p53 pathways may reveal important implications for the understanding of the role of IFN during carcinogenesis.