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Based on available literature and our experimental data, we develop a mathematical model of virus- and dsRNA-triggered signaling pathways leading to type I IFN gene expression during the primary response, and use the genetic algorithm to optimize all rate constants in the model.
We consider this model as a model of virus dynamics depicted in [46].
In the previous section, we analyzed the global stability of a model of virus infection with diffusion and time delay.
They presented a model of virus dynamics that can be further extended to include essential components of the cellular and humoral immune response.
We have previously introduced a novel model of virus dynamics and adaptation [23], which allows us to consider the distinct molecular effects of all novel (and some developmental) HIV drugs.
These assumption define the basic model of virus dynamics.
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Although preventive vaccination and specific therapies are yet to be developed, exploring this interesting model of virus-host interactions might have a strong effect on the design of novel therapeutic options to minimize immunopathology without impairing beneficial host defenses.
To exmine the feasibility of virus-encoded mimic epitopes to initiate CNS autoimmunity, we recently developed a molecular mimicry model of virus-induced demyelinating disease wherein a non-pathogenic variant strain of TMEV was engineered to encode a 30-mer peptide encompassing the immunodominant myelin proteolipid protein, PLP139 151, epitope.
We conclude that Twist contributes to EMT in the model of virus-induced pulmonary fibrosis.
Recently, we turned our attention to the factors that control fibroblast proliferation in this model of virus-induced lung fibrosis.
We used B cells incubated with formaldehyde-inactivated non-replicating influenza virus as a model of virus-containing cells, henceforth referred to as "flu-B cells".
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