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A mathematical model of the intracellular reproduction of the influenza virus has been constructed, which describes the regulation of transcription, translation, replication, and assembly of the virus in a sensitive noninterferonogenic cell. A structural and parametric verification of the model has been performed, which involves an analysis of alternative mechanisms of regulation of the key events of the reproduction of the influenza virus at the stages of the primary and secondary transcription. It was shown that the dynamics of the concentrations of the system components is in qualitative agreement with the experimental data. An analysis of the model parameters showed a high sensitivity of the model to changes in the parameters that control the efficiency of the binding of the viral polymerase to virus-specific RNAs at the stages of initiation and elongation of transcription and replication of the viral genome. The results obtained suggest that the stages of the virus reproduction sensitive to changes in the parameters are potential targets for drugs. Using the model, a minimal multiplicity of infection at which the formation of viral particles is observed was predicted.

Regulation of plant growth and development by auxin is mediated by the hormone controlled distribution and dose-dependent mechanisms of its action. A mathematical model is proposed, which described the distribution of auxin in the cells extending along the central axis of the Arabidopsis thaliana root. This model reproduces qualitatively both auxin distribution in cells of the root central axis under the normal conditions and under the conditions of decreased active transport and the recovery of auxin distribution and related meristem restoration during root regeneration after ablation of its tip. Different types of distribution of the auxin concentration over the vertical root axis are described, possible variants of root growth and lateral roots formation are proposed, and biological interpretation is given to different regimes of model behavior.