BackgroundHepatitis E virus (HEV) is a member of the Hepeviridae family; it has four main genotypes and one serotype. While genotypes 1 and 2 cause epidemic hepatitis and are transmitted via water and the fecal-oral route, genotypes 3 and 4 are zoonotic. In the various seroprevalence studies of hepatitis E in Brazil, the numbers reported vary widely and are difficult to interpret. The aim of this study was to analyze existing seroprevalence studies of hepatitis E in adults in Brazil.Main textWe searched the PubMed, Latin American and Caribbean Health Sciences and Embase databases for studies published from inception to May 12, 2018 concerning infection by HEV in Brazil without time period or language restrictions. We included studies that presented data concerning hepatitis E seroprevalence in adults in Brazil, had a sample size ≥50 patients and whose method used for the detection of anti-HEV was standardized and commercialized. We also evaluated the quality of the articles using a list of criteria that totalized 9 items. Of the 20 studies ultimately analyzed, 10 (50%) were from the southeast region of Brazil, 3 (15%) were from the central-west region, 3 (15%) were from the northern region, 2 (10%) were from the northeast region and 2 (10%) were from the southern region. Regarding the quality evaluation of the studies, the mean score was 5.6 (range: 4–8). The estimated overall seroprevalence of HEV infection in the adult population was 6.0% (95% CI: 5.0–7.0); in subgroup analyses, we observed that the prevalence of anti-HEV antibodies in blood donors was 7.0% (95% CI: 5.0–8.0), whereas in the general population, it was 3.0% (95% CI: 2.0–4.0).ConclusionsThe results of this systematic review indicate that there should be national investment in the prevention of hepatitis E virus infection in Brazil, including the implementation of improvements in basic sanitation and guidance regarding the appropriate handling of animal waste and the optimal cooking of vegetables, meat and their derivatives.Electronic supplementary materialThe online version of this article (10.1186/s40249-018-0514-4) contains supplementary material, which is available to authorized users.

BackgroundIn chronic hepatitis C, the fibrosis progression rates are extremely variable and can be influenced by factors associated with the host, virus and environment. Among the associated metabolic factors, hepatic steatosis is characterized by an accumulation of triglycerides in hepatocytes. In the host, genetic determinants of hepatic steatosis are observed, such as single-nucleotide polymorphisms (SNPs) in the microsomal triglyceride transfer protein (MTTP) gene. The MTTP -493G/T SNP appears to play an important role in the regulation of gene expression and influences the plasma concentration of circulating low-density lipoprotein (LDL). The present study investigated the influence of this SNP in the development of hepatic steatosis in patients with chronic hepatitis C and evaluated the association of hepatic steatosis with certain characteristics of these patients and the hepatitis C virus (HCV).MethodsTwo hundred thirty-nine patients with chronic hepatitis C were genotyped for the MTTP -493G⁄T SNP by a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. The association between hepatic steatosis and selected characteristics of the patient and virus was evaluated using bivariate and multivariate analyses.ResultsThe most prevalent MTTP -493G/T genotype was GG (46%) followed by GT (43.5%) and TT (10.5%). Multivariate analysis of the total cohort revealed associations between the presence of hepatic steatosis and inflammatory activity of moderate to high intensity (P < 0.001), advanced age (P = 0.010), elevated gamma glutamyl transpeptidase (GGT) levels (P = 0.010) and low LDL levels (P = 0.022). Hepatic steatosis was also associated with the TT/GT genotype of the MTTP -493G⁄T SNP in patients infected with HCV genotype 3 (P < 0.001).ConclusionsIn chronic hepatitis C patients infected with HCV genotype 3 and with the TT/GT genotype of the MTTP -493G/T SNP, a significant increase in hepatic steatosis was observed, which may indicate that this SNP has a significant influence on the accumulation of triglycerides in hepatocytes. Furthermore, associations were observed between hepatic steatosis and inflammatory activity of moderate to high intensity, advanced age, elevated GGT and low LDL levels.

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Aims To investigate the prevalence of hepatitis B virus (HBV) infection among alcohol users. Methods A systematic search of articles in the PubMed, Web of Science and EMBASE databases was conducted. The methodological quality of each study was scored, and a meta-analysis was performed taking into account the heterogeneity expected among the studies. Publication bias was assessed using Begg’s and Egger’s tests. Results The search identified 998 reports that yielded 18 eligible studies. The studies comprised 12,204 alcohol users, who were mostly men. The mean score on the quality evaluation was 6.9, and 11 studies were classified as having a low risk of bias. The estimated worldwide prevalence of HBV was 20.0% (95%CI: 19.0–20.0). The heterogeneity among the studies was substantial (I2 = 96.7%). In subgroup analyses, it was observed that among alcohol user dependents with no description of liver damage, alcohol users with different stages of chronic liver disease and alcohol users who all had cirrhosis, the estimated prevalence was 10.0% (95%CI: 8.0–14.0), 14.0% (95%CI: 13.0–15.0) and 32.0% (95%CI: 29.0–35.0), respectively. The meta-regression analysis showed that the study quality score had an influence on the investigated prevalence (P = 0.005). Nevertheless, the funnel plot showed asymmetry, and there was evidence of publication bias according to Egger’s test (P = 0.003) but not Begg’s test (P = 0.869). Conclusions The prevalence of HBV among alcohol users was high. HBV infection and alcohol consumption are factors affecting the development and worsening of liver disease; therefore, we suggest that adult alcohol users should be carefully monitored.

Several factors are associated with the progression of chronic hepatitis C: comorbidities, lifestyle, and pathogenic factors, including immune response, apoptosis and heredity. Single nucleotide polymorphisms (SNPs) in the PNPLA3 and TM6SF2 genes are more widely studied genetic risk factors, while CXCL9–11 chemokines produced by hepatocytes in the process of infection are less well studied. Our aim was to evaluate the influence of CXCL9 rs10336, CXCL10 rs3921 and CXCL11 rs4619915 in liver fibrosis when analysed together with PNPLA3 rs738409 and TM6SF2 rs58542926. The study included 219 patients with chronic hepatitis C. SNP genotyping was performed by real-time PCR. Univariate and multivariate analyses were used to detect the association between SNPs and advanced fibrosis in a recessive genetic model. All SNPs had a minimum allele frequency &gt; 5%, and CXCL9 rs10336, CXCL10 rs3921 and CXCL11 rs4619915 were in high linkage disequilibrium (D’ ≥0.84). In the multivariate analysis, we observed that male gender (p = 0.000), older age (p = 0.025), moderate to intense inflammatory activity (p = 0.002), moderate to accentuated hepatic steatosis (p = 0.026) and the CT genotype of the TM6SF2 rs58542926 SNP (p = 0.014) presented significant associations with advanced fibrosis. Overall, the CXCL9 rs10336, CXCL10 rs3921, CXCL11 rs4619915 and PNPLA3 rs738409 SNPs did not influence liver fibrosis among patients with chronic hepatitis C.

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