BackgroundPlasmodium vivax malaria clinical outcomes are a consequence of the interaction of multiple parasite, environmental and host factors. The host molecular and genetic determinants driving susceptibility to disease severity in this infection are largely unknown. Here, a network analysis of large-scale data from a significant number of individuals with different clinical presentations of P. vivax malaria was performed in an attempt to identify patterns of association between various candidate biomarkers and the clinical outcomes.MethodsA retrospective analysis of 530 individuals from the Brazilian Amazon, including P. vivax-infected individuals who developed different clinical outcomes (148 asymptomatic malaria, 187 symptomatic malaria, 13 severe non-lethal malaria, and six severe lethal malaria) as well as 176 non-infected controls, was performed. Plasma levels of liver transaminases, bilirubins, creatinine, fibrinogen, C-reactive protein, superoxide dismutase (SOD)-1, haem oxygenase (HO)-1 and a panel composed by multiple cytokines and chemokines were measured and compared between the different clinical groups using network analysis.ResultsNon-infected individuals displayed several statistically significant interactions in the networks, including associations between the levels of IL-10 and IL-4 with the chemokine CXCL9. Individuals with asymptomatic malaria displayed multiple significant interactions involving IL-4. Subjects with mild or severe non-lethal malaria displayed substantial loss of interactions in the networks and TNF had significant associations more frequently with other parameters. Cases of lethal P. vivax malaria infection were associated with significant interactions between TNF ALT, HO-1 and SOD-1.ConclusionsThe findings imply that clinical immunity to P. vivax malaria is associated with multiple significant interactions in the network, mostly involving IL-4, while lethality is linked to a systematic reduction of complexity of these interactions and to an increase in connections between markers linked to haemolysis-induced damage.

The genotypes of hepatitis B (HBV) and delta (HDV) viruses circulating among fulminant hepatitis cases from the western Amazon Basin of Brazil were characterized in this study. HBV and HDV isolates were obtained from liver samples from 14 patients who developed fulminant hepatitis and died during [1978][1979][1980][1981][1982][1983][1984][1985][1986][1987][1988][1989]. HBV DNA and HDV RNA were detected in all samples. Phylogenetic analyses of HDV sequences showed that they all clustered with previously characterized sequences of HDV genotype 3 (HDV-3). HBV genotypes F, A and D were found in 50.0, 28.6 and 21.4 % of cases, respectively. These results confirm the predominance of HDV-3 in South America and its association with the severe form of hepatitis, and the finding of the co-infection of HDV-3 with different genotypes of HBV suggests that the association between HDV-3 and HBV-F is not necessarily causally related to a more severe clinical course of infection.The Brazilian western Amazon Basin is considered a highly endemic area for hepatitis B (HBV) and delta (HDV) viruses (Bensabath & Dias, 1983; Bensabath et al., 1987;Braga et al., 2001;Fonseca et al., 1988;Viana et al., 2005). Severe hepatitis cases with peculiar clinical and histopathological features have been reported in this region. Cases of fulminant hepatitis with similar features have been described in other countries in northern South America (Colombia, Venezuela, Peru and Ecuador) and in the Central African Republic. This severe form of liver disease has been identified as HBV and HDV super-or coinfection (Bensabath et al., 1987; Buitrago et al., 1986;Casey, 1996;Casey et al., 1996; Hadler et al., 1984;Lesbordes et al., 1987;Ljunggren et al., 1985;Manock et al., 2000;Popper et al., 1983;Sjogren & Colichon, 1991;Torres & Mondolfi, 1991).The disease associated with HDV infection is typically more severe than that due to HBV infection alone, but its clinical spectrum ranges from asymptomatic carriage of the virus to very severe disease. A factor that may influence the course of disease is the genetical heterogeneity of HDV prevalent in different geographical areas (Casey, 1996;Rizzetto & Durazzo, 1991;Smedile et al., 1982). Only HDV genotype 3 (HDV-3) was identified in cases of fulminant hepatitis from different countries of South America and has been associated with the co-infecting HBV genotype F (HBV-F), which is also indigenous to South America, suggesting that HDV-3 alone or in combination with HBV-F could be an important determinant of the particularly severe form of HDV-related disease in this region (Casey, 1996;Nakano et al., 2001a, b). Bensabath et al. (1987) carried out a 5 year protocol during 1979-1984 in the Brazilian western Amazon Basin to study the epidemiology of HDV infection and its role in the aetiology of fulminant hepatitis. In that study, the authors observed a high endemicity of HBV and HDV infection and confirmed the presence of HDV as a major factor forThe GenBank/EMBL/DDBJ accession numbers for the sequences reported in ...

Vaccination coverage is decreasing worldwide, favoring the potential reemergence of vaccinepreventable diseases. In this study, we performed a longitudinal characterization of vaccination coverage in Brazil and compared the profiles between the distinct regions in the country to test whether there has been a substantial change over the last 5 years. Methods: De-identified publicly available data were retrieved from the repository of the Brazilian Ministry of Health, comprising detailed information on vaccination coverage in all age groups between 1994 and 2019. The vaccination coverage for the whole country and for each Brazilian region, by year, was examined, and a time-series pattern analysis was performed. Results: A significant decrease in overall vaccination coverage across the country regions was observed between 2017 and 2019, especially in childhood immunization. A reduction in BCG, hepatitis B, influenza, and rotavirus vaccine coverage was observed. Conversely, vaccines against measles, mumps, rubella, varicella, and meningococcus showed an increase in coverage. Region-specific changes in vaccination patterns within the study period were observed. Conclusions: A substantial reduction in vaccination coverage was detected in Brazil, a country already highly susceptible to the emergence of epidemic infectious diseases. Continuing evaluation of the immunization program actions may help to improve vaccination coverage and prevent new epidemics.

This study aims to describe the oral microbiome diversity and prevalence of ARGs in periodontal health and disease. Background The human oral cavity harbors a complex microbial community known as the oral microbiome. These organisms are regularly exposed to selective pressures, such as the usage of antibiotics, which drive evolution and acquisition of antibiotic resistance genes (ARGs). Resistance among oral bacteria jeopardizes not only antibiotic therapy for oral infections, but also extra-oral infections caused by bacterial translocation. Methods We carried out a cross-sectional investigation. Saliva and subgingival plaque samples were collected during a clinical exam. 16S rRNA gene sequencing was performed to assess microbial diversity. Resistance genes were identified through PCR assays. Results Of the 110 participants, only 22.7% had healthy periodontium, while the majority was diagnosed with gingivitis (55.4%) and chronic periodontitis (21.8%). The composition of the oral microbiota differed from healthy and diseased samples, being Streptococcus spp. and Rothia spp. predominant in periodontal disease. Regarding ARGs, 80 (72.7%) samples were positive for at least one of genes screened, erm being the most frequent variant (58.2%), followed by bla TEM (16.4%), mecA (2.7%), pbp2b and aac(6 ') (1.8%). Neither genes coding resistance to carbapenems nor metronidazole were detected. Conclusions Our findings indicate that there are no significant differences in terms of taxonomic enrichment between healthy and diseased oral microbiomes. However, samples retrieved from healthy patients had a more diverse microbial community, whereas diseased samples have

There is currently no system to track the emergence of Zika virus (ZIKV) subtypes. We developed a surveillance system able to retrieve sequence submissions and further classify distinct ZIKV genotypes in the world. This approach was able to detect a new occurrence of ZIKV from an African lineage in Brazil in 2019.