Host Immune Recognition, Pattern Recognition Receptor Signaling, and Antigen Presentation Pathways Initiating Chronic Host–Pathogen Interactions
Keywords:
Viral Infection,Abstract
Background: The spread of chronic viral diseases like Hepatitis B (HBV) and Human Immunodeficiency Virus (HIV) became a significant health issue in the world. Pattern recognition receptor (PRR) signaling, antigen presentation pathways (APP), and host immune recognition (HIR) were the key pathways of host immune response that were often dysregulated to allow viral persistence. This study aimed at synthesizing available literature on the dysregulation of PRR signaling, HIR and APP pathways in the development and persistence of chronic HBV and HIV infections. Methods: This study was performed according to PRISMA 2020 guidelines. Research was conducted in PubMed, Scopus, Web of Science, and Google Scholar from 2014 to 2024. Those studies included that involved PRR (e.g. TLRs), HIR (e.g. T cell subsets), and APP (e.g. dendritic cell function) interactions in the chronic HBV and HIV. Non-English articles, reviews, and studies without quantitative data were excluded. Statistical analyses were performed using MetaAnalysisOnline tool. The risk of bias was assessed using appropriate tools, and the certainty of evidence was evaluated using the GRADE framework. Results: The analysis of twelve studies revealed downregulation of TLR7 (SMD: -1.92, 95% CI: -3.19 to -0.66) and reduction of CD3⁺ T cells (SMD: -1.95, 95% CI: -3.36 to -0.55) in patient cohorts versus controls, whereasTLR2, TLR4, CD4⁺, CD8⁺ T, and dendritic cell markers showed no statistically association. Overall risk of bias was evaluated to be moderate, whereas the certainty of evidence was low. Conclusion: Chronic infections were characterized by parallel dysfunctions across PRR signaling, adaptive HIR, and APP.
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