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Objective: To investigate the carriage of HBs antigen (Ag) and hepatitis C virus in people with human immunodeficiency virus (HIV) at Grand-Yoff General Hospital. Materials and Methods: Sera from patients living with HIV and monitored at Grand-Yoff General Hospital have benefited from research for HBs Ag, HBe Ag, anti-H[8] Be antibodies and on these co-infected patients, a test for hepatitis C virus was also carried out. Results: This study included 147 HIV-infected patients and including 95 women (64.63%) and 52 men (35, 37%) with a median age of 46 years (16-78 years). The gender ratio is M/W was 0.54 and the age group most represented at inclusion was 30-39 years old with 31.97% of patients. 12, 25% of patients were co-infected HIV and hepatitis B including 11 women (61.11%) and 7 men (38.89%). The median age was 39.5 years (33-60 years), women were the affected by co-infection and 44.44% of them were married. Chronic hepatitis B and hepatitis C markers were tested for in HIV/HBV coinfected patients using a microparticulate chemiluminescence immunoassay technic. Investigation of hepatitis B chronicity markers indicated that all patient, except one, underwent anti-HBe seroconversion (94.4%) and no case of co-infection with HCV had been noted. During follow-up, all patients were under antiretroviral therapy with mainly tenofovir (TDF) which was the most used molecule with 83.33%, followed by lamivudine (3TC) 16.67%. Conclusion: HIV infection is a major public health problem when it is associated with hepatitis B and C virus.

Malaria infection is a multifactorial disease partly modulated by host immuno-genetic factors. Recent evidence has demonstrated the importance of Interleukin-17 family proinflammatory cytokines and their genetic variants in host immunity. However, limited knowledge exists about their role in parasitic infections such as malaria. We aimed to investigate IL-17A serum levels in patients with severe and uncomplicated malaria, whether IL-17A gene polymorphisms are involved in severe malaria susceptibility and the polymorphism’s influence on the IL-17A serum levels. 125 malaria patients and 48 free malaria controls were enrolled in this research. Malaria patients were classified into severe malaria (SM) and uncomplicated malaria (UM). IL-17A serum levels were measured with ELISA. PCR and DNA sequencing were used to assess host genetic polymorphisms in IL-17A. We performed a multivariate regression to estimate the impact of human IL-17A variants on IL-17A serum level and malaria outcome. Elevated serum IL-17A levels accompanied by increased parasitemia were found in SM patients compared to UM and controls (P

BackgroundThe first discovery of Plasmodium vivax infections in Senegal used archived patients’ sera in place of blood pellet, the preferred specimen for the molecular diagnosis of Plasmodium species. The present study assessed the reliability of detecting P. vivax DNA in plasma in comparison to blood pellet from the same patient’s samples.MethodsA total of 616 blood samples obtained from febrile patients living in Kolda (2015 and 2020), Tambacounda (2017 and 2020), and Kedougou (2020) regions in Senegal, were first screened for Plasmodium species composition by 18S ssrRNA-based nested PCR. Paired blood pellets and plasma samples were selected from a subset of 50 P. vivax-positive patients matched by age and sex with 50 P. vivax-negative patients, and subjected to a cytochrome b-based qPCR to compare the detection and quantification of P. vivax genomic DNA between the two specimen types.Results and discussionThe study reports 1.8% and 14.77% of single and mixed P. vivax infections in the study population, and a high concordance (84%) between the qPCR detection of P. vivax genomic DNA from paired blood pellets and plasma samples. Importantly, all P. vivax negative samples from the blood pellets were also confirmed plasma-negative, and parasitaemia in blood pellets was higher compared to plasma samples. The results support investigations of P. vivax infections in archived sera or plasma collections with a high degree of confidence to generate additional data on the neglected P. vivax malaria, and ultimately guide strategies to control the disease.

Galectin-3 is a member of the lectin family encoded by the LGALS3 gene on chromosome 14. It is secreted by a wide range of immune cells and mammary tumor cells. Through its activity on the tumor microenvironment, in particular on tumor-infiltrating leukocytes, galectin-3 improves the proliferation, survival, and colonizing ability of mammary neoplastic cells. Consequently, galectin-3 expression in the tumor microenvironment could worsen therapeutic outcomes of breast neoplasms and become a biomarker and a therapeutic target in combined immunotherapy in breast neoplasms. There is a limited amount of information that is available on galectin-3 in breast cancer in Africa. In this review, we analyze how galectin-3 influences the tumor microenvironment and its potential as a biomarker and therapeutic target in breast neoplasms. We aim to emphasize the significance of investigating galectin-3 in breast neoplasms in Africa based on the results of studies conducted elsewhere.

Genome-wide association studies for severe malaria (SM) have identified 30 genetic variants mostly located in non-coding regions. Here, we aimed to identify potential causal genetic variants located in these loci and demonstrate their functional activity. We systematically investigated the regulatory effect of the SNPs in linkage disequilibrium (LD) with the malaria-associated genetic variants. Annotating and prioritizing genetic variants led to the identification of a regulatory region containing five

Founder mutations have been reported in BRCA1 and BCRA2 in different ethnic groups with inherited breast cancer. Testing of targeted mutations in specific populations is important for cancer prevention in mutation carriers. In Sub-Saharan Africa, only a few studies have reported specific founder mutations in inherited breast cancer. The pathogenic variant c.815_824dup of BRCA1 has been reported as the most frequent among African American populations with inherited breast cancer and was supposed to have a West African origin. Recent report from Senegal identified this variant in women with inherited breast cancer at the highest frequency ever reported. The variant was linked to a common haplotype confirming its founder effect in West Africa. In this article, we review the mutation history of c.815_824dup and discuss how it spread out of Africa through the transatlantic slave trade.