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• W2228163526 abstract "Abstract Purpose The complex interactions between genetic machinery of HIV-1 and host immune cells mediate dynamic adaptive responses leading to Autoimmune Deficiency Syndrome. These interactions are captured as Biological Regulatory Network (BRN) which acts to maintain the viability of host cell machinery through feedback control mechanism which is a characteristic of complex adaptive systems. In this study, the BRN of immune response against HIV-1 infection is modeled to investigate the role of NF-κB and TNF-α in disease transmission using qualitative (discrete) and hybrid modeling formalisms. Methods Qualitative and Hybrid modeling approaches are used to model the BRN for the dynamic analysis. The qualitative model is based on the logical parameters while the hybrid model is based on the time delay parameters. Results The qualitative model gives useful insights about the physiological condition observed as the homeostasis of all the entities of the BRN as well as pathophysiological behaviors representing high expression levels of NF-κB, TNF-α and HIV. Since the qualitative model is time abstracted, so a hybrid model is developed to analyze the behavior of the BRN by associating activation and inhibition time delays with each entity. HyTech tool synthesizes time delay constraints for the existence of homeostasis. Conclusion Hybrid model reveals various viability constraints that characterize the conditional existence of cyclic states (homeostasis). The resultant relations suggest larger cycle period of HIV-1 than the cycle periods of the other two entities (NF-κB and TNF-α) to maintain a homeostatic expressions of these entities." @default.
• W2228163526 created "2016-06-24" @default.
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• W2228163526 date "2016-01-08" @default.
• W2228163526 modified "2023-10-11" @default.
• W2228163526 title "On the modeling and analysis of the biological regulatory network of NF-$${kappa }$$B activation in HIV-1 infection" @default.
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• W2228163526 doi "https://doi.org/10.1186/s40294-015-0013-4" @default.
• W2228163526 hasPublicationYear "2016" @default.
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