scholarly journals Regulation of Organism's Antiviral Immune Response: Mathematical Model, Qualitative Analysis, Results

Author(s):  
P.V. Trusov ◽  
N.V. Zaitseva ◽  
V.M. Chigvintsev ◽  
D.V. Lanin

To know the processes occurring in the neuroendocrine and immune system, the complex and branching regulation mechanisms should be taken into account. Most of the studies in this area are dedicated to the biological and mathematical description of individual parts of the regulatory mechanisms, and it greatly facilitates the understanding of the phenomena being studied. But there is a lack of comprehensive description of the processes and internal communications. In the present article, a mathematical model for describing the antiviral immune response is considered taking into account the interacting regulatory influences of the immune and neuroendocrine systems. To describe the innate immunity, the proposed model uses parameters reflecting quantitative measures of the interferon concentration (the inductor of resistance to the infection of target organ cells) and NK-cells (responsible for removing of the infected cells). The simulation of acquired immunity is performed using parameters characterizing the concentration of virus-specific cytotoxic T cells and antibody-forming B lymphocytes. The regulatory mechanisms considered in the model cover the influence of the hypothalamic-pituitary-adrenal axis and the populations of the T-helper cells. The model is developed within the framework of the concept of a multi-level model of the human body, taking into account the interactions between systems and the functional state of the organs included in the review. The model also takes into account the spatial organization of immune and infectious processes in various organs and tissues, for which the delay time of interaction of the components is introduced. The model includes a system of 18 ordinary differential equations with a delayed argument, the parameters of which characterize the rates of various processes that affect the dynamics of infection. The parameters are identified according to published experimental data describing the process of infection of the body with a virus. The dynamics of the immune and neuroendocrine systems under viral infection was calculated, taking into account the disturbance of the synthetic function of the bone marrow. The study provides a qualitative picture of the biological factors that can explain the kinetics of the development of a viral infection.

The innate immune response to viral pathogens is crucial in mobilizing defensive reactions of an organism during the development of an acute viral infection. Cells of the innate immunity system detect viral antigens due to genetically programmed pattern-recognition receptors (PRRs), which are located either on the cell surface or inside the certain intracellular components. These image-recognizing receptors include Toll-like receptors (TLRs), retinoic acid-inducible gene I-like receptors (RIG-I-like receptors), nucleotide oligomerization domain-like receptors (NOD-like receptors), also known as NACHT, LRR and PYD domains of the protein, and cytosolic DNA sensors. The trigger mechanisms for these receptors are viral proteins, and nucleic acids serve as activators. The presence of PRRs that are responsible for the determination of viral antigens in cellular components allows the cells of innate immunity to recognize a wide range of viral agents that replicate in various cellular structures, and develop an immune response to them. This article summarizes the disparate data presented in modern English literature on the role of PRRs and the associated signaling pathways. Understanding the recognition of viral pathogens required triggering a cascade of cytokine and interferon production provides insights into how viruses activate the signal paths of PRRs and the effect of the interaction of viral antigens and these receptors on the formation of the antiviral immune response.


Author(s):  
Novianti Anggie Lestari ◽  
Dwi Retnoningrum

Coronavirus 2019 (COVID-19) is an infectious disease caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Inflammation occurs when the body is infected with the virus. Platelets play a role in immune response and immunomodulation by activating P-Selectin Glycoprotein (PSGL) to the site of inflammation. Lymphocytes play a role through CD4 T-cells, B-cells producing specific viral antibodies, and CD8 cytotoxic T-cells by directly killing the virus in infected cells. This study aimed to prove the correlation between PLR and CRP as inflammation markers in COVID-19 patients. This study was a retrospective observational study with the cross-sectional approach at Dr. Kariadi Hospital, Semarang, for the period March-August 2020. Spearman test performed for analyzing data with p<0.05 was significant. Thirty-three confirmed COVID-19 patients with median value of PLR 218 (103-1609) and CRP 15.94 (1.24-200) mg/L were tested for correlation with a value of p=0.013 and r=0.427. The increase of PLR and CRP in COVID-19 patients was caused by an inflammatory process mediated by the immune response. High values in the blood were associated with disease severity and poor prognosis. There was a statistically significant moderate positive correlation between PLR and CRP in COVID-19 patients.


2021 ◽  
Vol 12 ◽  
Author(s):  
Fei Wang

Viral infection triggers insect immune response, including RNA interference, apoptosis and autophagy, and profoundly changes the gene expression profiles in infected cells. Although intracellular degradation is crucial for restricting viral infection, intercellular communication is required to mount a robust systemic immune response. This review focuses on recent advances in understanding the intercellular communications in insect antiviral immunity, including protein-based and virus-derived RNA based cell-cell communications, with emphasis on the signaling pathway that induces the production of the potential cytokines. The prospects and challenges of future work are also discussed.


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