People who use crack-cocaine (PWUCC) have numerous vulnerabilities and pose a challenge to health and social assistance services. The exposure to pathogens and risk situations occur differently according to each individual, region and social group. This study identified the presence, genotypes and factors associated with hepatitis E virus (HEV) exposure among a community-recruited cohort of 437 PWUCC in northern Brazil. Epidemiological information was collected through community-based assessments and interviews. Thereafter, blood and fecal samples were collected and tested for HEV using an immunoenzymatic assay, and the genotype was identified by PCR. Logistic regressions were used to identify the risk factors independently associated with exposure to HEV. In total, 79 (18.1%) PWUCC were exposed to HEV: 73 (16.7%) for IgG and six for IgG + IgM. HEV RNA was detected in six fecal samples and in two blood samples from PWUCC with IgM + IgG. Subtype 3c was identified in all of the samples. The factors associated with exposure to HEV were low monthly income, unstable housing (e.g., homelessness), crack-cocaine use ≥40 months, and the shared use of crack-cocaine equipment. The current study provides unique initial insights into HEV status and risk factors among PWUCC in a remote area in Brazil, with diverse implications for urgently improved diagnosis, prevention, and treatment intervention needs.

Coinfection of HPgV-1 with hepatitis C virus (HCV) is common due to shared modes of transmission, with a prevalence of HPgV-1 viremia of approximately 20% among individuals with chronic HCV infection. The aim of the present study was to estimate the prevalence of HPgV-1 RNA and circulating genotypes in patients with hepatitis C from a health service located in the city of Belém, in the state of Pará, Northern Brazil. A total of 147 samples were included in the study from February to December 2019. Among the participants, 72.1% (106/147) were monoinfected with HCV, with detectable HCV viral RNA, and 27.9% (41/147) were coinfected with HCV/HPgV-1. The most frequently found genotypes were HPgV-1 genotypes 1 and 2 (36.6% and 63.4%), respectively. While for HCV there was a predominance of genotypes 1 and 3 (58.5% and 41.5%). No significant differences were found when comparing any risk, sociodemographic, or clinical factors between groups. Also, there was no statistically significant difference when relating the viral genotypes of both agents. This study indicated that the prevalence of infection by HPgV-1 is high in HCV carriers in Belém, Pará, and probably does not change the clinical course of HCV infection, however, further studies are still needed.

Hepatitis B and C are the most common causes of liver disease worldwide. The two infections share many similarities such as a global distribution, the same routes of transmission, hepatotropism, and the ability to cause chronic infection. The consequences of HBV/HCV coinfection are still being studied. The aim of this study is to describe and compare the epidemiological and laboratory profile and the degree of hepatic fibrosis between HCV-monoinfected and HBV/HCV-coinfected patients in the Brazilian Amazon region. ELISA tests were used for the investigation of HBV and HCV serological markers, and molecular tests were used for the detection and genotyping of these viruses. Additionally, transaminases were measured, and a FibroScan was performed for the analysis of liver function. A total of 328 patients with HCV participated in the study. The serological prevalence of HCV/HBV coinfection was 10.77%. A comparison of risk factors between the monoinfected and coinfected groups showed that illicit drug use, sharing sharp instruments, and tattooing/piercing are significantly associated with coinfection. The monoinfected patients had a higher HCV load than the coinfected patients. A viral interaction was observed in this study in which the presence of a coinfection with HBV appears to influence HCV replication. Further studies are necessary to better understand this interaction.

Acute lymphoblastic leukemia (ALL) is an aggressive neoplasm derived from B and/or T cell lineage (B-ALL; T-ALL). For the first time, this study describes, cytogenetically, the karyotypic alterations in adults with ALL in the northern region of Brazil and their relationship with hematological and biochemical characteristics. Through banding analyses, immunophenotyping, as well as hematological and biochemical examination data obtained directly from patients’ records, we found that chromosome 21 aneuploidy was the most frequent. The cytogenetic structural alterations observed with the highest incidence among the patients were: t(9;22), t(4;11), t(1;19), del(6q), and del(9p). In patients presenting with chromosome alterations, we verified that patients with t(4;11) have elevated red blood cell levels and patients with del(9p) presented with distinct and high values of hematological parameters compared to other patients. Regarding biochemical alterations, we observed that patients with translocations (4;11) and del(6q) presented with elevated urea levels compared to other patients, highlighting its relationship to kidney changes and patient prognosis. Thus, our study highlights that variations in hematological and biochemical data are associated with specific cytogenetic changes and other factors, which may impact the prognosis of adult patients with ALL.

Infections with the Hepatitis B (HBV) and Hepatitis C (HCV) viruses share some transmission routes, which is why coinfection with these viruses becomes common, especially in endemic areas. This study evaluated the immunological response profile, viral load, and liver damage in groups monoinfected with HBV or HCV and in those co-infected with HBV/HCV. The groups were composed of 22 patients monoinfected by HCV, 22 patients monoinfected by HBV, and 34 co-infected by HBV/HCV, according to serological markers and molecular biology tests. The study was carried out from December 2017 to October 2019. Virus detection employed enzyme immunoassay, Enzyme-Linked Immunosorbent Assay (ELISA), and real-time PCR, while liver function and fibrosis were assessed using biochemical tests and Fibroscan. To research the immunological profile, cytokines were quantified using the BIO-Plex Pro Human Cytokine. Comparing the groups, both mono- and co-infected patients exhibited a Th1 immune response profile. HCV monoinfection notably showed significantly elevated serum levels of INF-γ (p < 0.01) and TNF-α (p < 0.01). The viral load was significantly higher in the HCV monoinfected group when compared to the other groups. Regarding liver damage, patients with a high level of fibrosis (F4) presented significant levels of cytokines INF-γ (p < 0.001), IL-17 (p < 0.0001), and TNF-α (p < 0.0001).

The Philadelphia (Ph+) chromosome, t(9;22)(q34;q11.2), originates from a chimeric gene called BCR-ABL and is present in more than 90% of CML patients. Most patients with CML express the protein p210 BCR-ABL and, with a frequency lower than 5%, express rare isoforms, the main one being p190. In the transition from the chronic phase to the blast phase (BP), additional chromosomal abnormalities, such as the presence of the double Ph+ chromosome, are revealed. Of the 1132 patients analyzed via molecular biology in this study, two patients (0.17%) showed the co-expression of the p210 and p190 isoforms for the BCR-ABL transcript, with the concomitant presence of a double Ph+ chromosome, which was observed via conventional cytogenetics and confirmed by fluorescent in situ hybridization. The BCR-ABL/ABL% p210 and p190 ratio increased in these two patients from diagnosis to progression to blast crisis. To our knowledge, this is the first report in the literature of patients who co-expressed the two main BCR-ABL transcript isoforms and concomitantly presented Ph+ chromosome duplication. The evolution from the chronic phase to BP often occurs within 5 to 7 years, and, in this study, the evolution to BP was earlier, since disease-free survival was on average 4.5 months and overall survival was on average 9.5 months. The presence of the p190 transcript and the double Ph+ chromosome in CML may be related to the vertiginous progression of the disease.