Introduction: Malaria molecular surveillance (MMS) can provide insights into transmission dynamics, guiding national control programs. We previously designed AmpliSeq assays for MMS, which include different traits of interest (resistance markers and deletions), and SNP barcodes to provide population genetics estimates of and parasites in the Peruvian Amazon. The present study compares the genetic resolution of the barcodes in the AmpliSeq assays with widely used microsatellite (MS) panels to investigate population genetics of Amazonian malaria parasites.
View Article and Find Full Text PDFChikungunya virus infection (CHIKV) increases the risk of persistent arthralgia; however, there is no consistent evidence regarding prognostic biomarkers of progression to chronic arthropathy. This systematic review provides an overview of currently available literature about the potential role of the acute immunologic response in predicting long-term joint pain in patients with a diagnosis of CHIKV. We searched for observational studies using the terms "chikungunya," "cytokines," "biomarkers," and "joint pain" in PubMed/MEDLINE, LILACS, Cochrane Library Plus, and SCOPUS databases, restricting to articles published in English and up to April 2024.
View Article and Find Full Text PDFBackground & Aims: Integrated HBV DNA (iDNA) plays a critical role in HBV pathogenesis, particularly in predicting treatment response and HCC. This study aimed to use an HBV hybridization-capture next-generation sequencing (HBV-NGS) assay to detect HBV-host junction sequences (HBV-JS) in a sensitive nonbiased manner to detect and estimate the iDNA fraction in tissue biopsies and HBV genetics by liquid biopsy.
Methods: HBV DNA from plasmid monomers, HBV-HCC cell line (SNU398, Hep3B, and PLC/PRF/5), tissue biopsies of patients with serum HBV DNA <4 log IU/ml, and matched urine and plasma of HBV patients were assessed by HBV-NGS.
MOTS-c is a mitochondrial microprotein that improves metabolism. Here, we demonstrate CK2 is a direct and functional target of MOTS-c. MOTS-c directly binds to CK2 and activates it in cell-free systems.
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