Hepatitis delta virus (HDV) has been associated with acute or chronic hepatitis in Latin America, but there is no prevalence study covering South American countries. This meta-analysis aimed to estimate anti-HDV prevalence through a systematic review of published articles in English, Portuguese and Spanish until December 2017. Searches were conducted in Health Virtual Library, Capes, Lilacs, PubMed, and SciELO, according to defined criteria regarding participant selection and geographical setting. Study quality was assessed using the GRADE guidelines. Pooled anti-HDV prevalence was calculated using the DerSimonian-Laird random-effects model with Freeman-Tukey double arcsine transformation. Out of the 405 identified articles, only 31 met the eligibility criteria for inclusion in the meta-analysis. In South America, pooled anti-HDV prevalence among hepatitis B virus carriers was 22.37% (95% confidence interval: 13.72-32.26), though it appeared less frequently in some countries and populations, according to the data collection date. The findings indicated significant successive reductions in anti-HDV prevalence over thirty years. However, there was a scarcity of HDV epidemiological studies outside the Amazon Basin, notably in the Southwest continent and absence of target population standardization. There was a high HDV prevalence in South American countries, despite differences in methodological characteristics and outcomes, highlighting a drastic decline in the last decades. Future studies should identify HDV prevalence estimates in other regions of the continent and identify risk factors.

Brucella, the etiological agent of animal and human brucellosis, is a bacterium with the capacity to modulate the inflammatory response. Cyclic β-1,2-glucan (CβG) is a virulence factor key for the pathogenesis of Brucella as it is involved in the intracellular life cycle of the bacteria. Using comparative studies with different CβG mutants of Brucella, cgs (CβG synthase), cgt (CβG transporter) and cgm (CβG modifier), we have identified different roles for this polysaccharide in Brucella. While anionic CβG is required for bacterial growth in low osmolarity conditions, the sole requirement for a successful Brucella interaction with mammalian host is its transport to periplasmic space. Our results uncover a new role for CβG in promoting splenomegaly in mice. We showed that CβG-dependent spleen inflammation is the consequence of massive cell recruitment (monocytes, dendritics cells and neutrophils) due to the induction of pro-inflammatory cytokines such as IL-12 and TNF-α and also that the reduced splenomegaly response observed with the cgs mutant is not the consequence of changes in expression levels of the characterized Brucella PAMPs LPS, flagellin or OMP16/19. Complementation of cgs mutant with purified CβG increased significantly spleen inflammation response suggesting a direct role for this polysaccharide.

Introduction: Leishmania infantum was considered to be absent from Amapá until 2017 when canine infection was detected. However, there is a lack of knowledge about which reservoir species are involved in transmission in this region.Methods: Between 2014 and 2016, 86 samples from wild mammals and 74 from domestic dogs were collected in Wajãpi Indigenous Territory and were tested for the presence of deoxyribonucleic acid (DNA) of Leishmania. Results: The DNA of Le. infantum was detected in two rodent samples, Dasyprocta sp. and Proechimys cuvieri. Conclusions: This is the first evidence characterizing a sylvatic transmission cycle of Le. infantum in the State of Amapá.

f Brucella species can cause brucellosis, a zoonotic disease that causes serious livestock economic losses and represents a public health threat. The mechanism of virulence of Brucella spp. is not yet fully understood. Therefore, it is crucial to identify new molecules that serve as virulence factors to better understand this host-pathogen interplay. Here, we evaluated the role of the Brucella membrane fusogenic protein (Mfp) and outer membrane protein 19 (Omp19) in bacterial pathogenesis. In this study, we showed that B. abortus ⌬mfp::kan and ⌬omp19::kan deletion mutant strains have reduced persistence in vivo in C57BL/6 and interferon regulatory factor 1 (IRF-1) knockout (KO) mice. Additionally, 24 h after macrophage infection with a ⌬mfp::kan or ⌬omp19::kan strain expressing green fluorescent protein (GFP) approximately 80% or 65% of Brucella-containing vacuoles (BCVs) retained the late endosomal/lysosomal marker LAMP-1, respectively, whereas around 60% of BCVs containing wild-type S2308 were found in LAMP-1-negative compartments. B. abortus ⌬omp19::kan was attenuated in vivo but had a residual virulence in C57BL/6 and IRF-1 KO mice, whereas the ⌬mfp::kan strain had a lower virulence in these same mouse models. Furthermore, ⌬mfp::kan and ⌬omp19::kan strains were used as live vaccines. Challenge experiments revealed that in C57BL/6 and IRF-1 KO mice, the ⌬mfp::kan strain induced greater protection than the vaccine RB51 and protection similar that of vaccine S19. However, a ⌬omp19::kan strain induced protection similar to that of RB51. Thus, these results demonstrate that Brucella Mfp and Omp19 are critical for full bacterial virulence and that the ⌬mfp::kan mutant may serve as a potential vaccine candidate in future studies. Brucellosis is a chronic infectious disease caused by bacteria of the genus Brucella. This disease affects many species of animals, resulting in great economic losses, and is therefore an important bacterial zoonotic disease worldwide (1). The genus Brucella replicates inside trophoblasts, macrophages, and dendritic cells and colonizes the reticuloendothelial system and reproductive organs (2). Additionally, brucellosis is not only the major cause of abortion and infertility in animals but also a debilitating disease in humans (2-7).To overcome the immune system and establish a chronic infection, B. abortus utilizes diverse evasion mechanisms. This pathogen can penetrate host cells through lipid rafts (8). Once inside cells, the establishment of a persistent infection relies on the ability of the bacterium to form a Brucella-containing vacuole (BCV), which traffics from the endocytic compartment to the endoplasmic reticulum (ER), forming a replicative BCV. It is in this replicative BCV that the bacteria begin to multiply (8, 9).Extensive vaccination programs have been undertaken to prevent brucellosis in animals. Despite their availability, live vaccine strains have critical disadvantages (10). The main vaccines currently available for brucellosis are S19 and RB51 (derived from B. abortus)...

No abstract