Hepatitis E virus (HEV) is worldwide distributed and might cause acute or chronic hepatitis mainly in immunocompromised individuals. In previous studies we found a high prevalence of antibodies to HEV within blood donors in south Brazil and also within backyard-raised pigs. Here we aimed to investigate the prevalence of anti-HEV antibody and HEV RNA within the general population from three major municipalities (Caxias do Sul, Passo Fundo and Santa Maria) in south Brazil. A total of 3,000 blood samples were randomly obtained from clinical laboratories at each of the three municipality (n = 1,000 each) to determine the presence of anti-HEV antibodies and HEV RNA. Overall, anti-HEV antibodies were detected in 574/1,000 (57,4%) samples in Caxias do Sul, 655/1,000 (65.5%) samples in Passo Fundo and 554/1,000 (55.4%) samples in Santa Maria. The prevalence of HEV-positive samples increased steadily and significantly (P < 0,001) with age and was unusually higher within individual over 40 years. Despite of this, none of the pooled serum samples had detectable levels of HEV RNA. The high anti-HEV antibody prevalence suggests that the virus might be present on the environment and/or foodstuff and poses a permanent threat to immune-compromised individuals.
Glaesserella parasuis is the etiological agent of Glässer’s disease (GD), one of the most important diseases afflicting pigs in the nursery phase. We analyzed the genetic and immunological properties of the TbpB protein naturally expressed by 27 different clinical isolates of G. parasuis that were typed as serovar 7 and isolated from pigs suffering from GD. All the strains were classified as virulent by LS-PCR. The phylogenetic analyses demonstrated high similarity within the amino acid sequence of TbpB from 24 clinical strains all belonging to cluster III of TbpB, as does the protective antigen TbpBY167A. Three G. parasuis isolates expressed cluster I TbpBs, indicating antigenic diversity within the SV7 group of G. parasuis. The antigenic analysis demonstrated the presence of common epitopes on all variants of the TbpB protein, which could be recognized by an in vitro analysis using pig IgG induced by a TbpBY167A-based vaccine. The proof of concept of the complete cross-protection between clusters I and III was performed in SPF pigs immunized with the TbpBY167A-based vaccine (cluster III) and challenged with G. parasuis SV7, strains LM 360.18 (cluster I). Additionally, pigs immunized with a whole-cell inactivated vaccine based on G. parasuis SV5 (Nagasaki strain) did not survive the challenge performed with SV7 (strain 360.18), demonstrating the absence of cross-protection between these two serovars. Based on these results, we propose that a properly formulated TbpBY167A-based vaccine may elicit a protective antibody response against all strains of G. parasuis SV7, despite TbpB antigenic diversity, and this might be extrapolated to other serovars. This result highlights the promising use of the TbpBY167A antigen in a future commercial vaccine for GD prevention.
Introduction: Nimesulide is a potent anti-inflammatorywith rapid and long-lasting effects, but also with a high riskof hepatotoxicity. Objective: This work aimed to preventnimesulide-induced hepatotoxicity through the associationof nimesulide with a hepatoprotective agent. Materials andMethods: First, we tested three hepatoprotective agents:N-acetylcysteine, L-carnitine, and Gingko biloba extract inan in vitro hepatic cell model. Both N-acetylcysteine and G.biloba showed promisor results. We selected N-acetylcysteineto continue the studies in an animal model. In vivo study wasperformed using male Wistar rats divided in 4 groups: control,nimesulide (100mg/kg/day), nimesulide (100mg/kg/day) +N-acetylcysteine (100mg/kg/day) and N-acetylcysteine alone(100mg/kg/day). Treatments were given by gavage, daily, for15 days. Results: Animals receiving nimesulide alone showedlower body weight gain compared to control. Body weightgain in the nimesulide + N-acetylcysteine group was higherthan nimesulide alone, evidencing lower toxicity. However,the body weight gain of the nimesulide + N-acetylcysteinegroup was still lower than the control animals. Animals treatedwith nimesulide alone presented an increased relative mass ofheart, liver, and spleen and significant hepatic damage seen inmicroscopy when compared to other groups. N-acetylcysteineco-administered with nimesulide prevented the increasedheart mass, but the same was not true with liver and spleen.Conclusions: This work evidence partial protection elicitedby the association of N-acetylcysteine and nimesulide againstnimesulide-induced hepatotoxicity.
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