Our observation that MC stabilization also promotes modestly increased viremia, at least when used in an immunocompromised mouse model where virus replication cannot be effectively controlled, also appears to support the contrasting role of MCs in the effective containment of DENV infection (St John et al., 2011), occurring in this case independent of interferon responses.
With regard to the time-dependent course of viral myocarditis, as studied in the mouse model, early virus-induced myocardial damage already takes place before the histopathological signs of myocarditis defined by the Dallas criteria can be observed [ 10, 16].
These results demonstrate that a live attenuated HSV-2 virus that lacks glycoprotein D (the main component of other failed vaccines) elicits a different type of immune response and is a safe and effective vaccine in mouse models of virus infection.
Then, in an in vitro model of vascular leak, the authors found that NS1 fractured the integrity of endothelial cell monolayers through a TLR4-dependent pathway, a finding that was supported by the observation that a TLR4 antagonist quelled capillary leak in a mouse model of dengue virus infection.
Similarly, an NKT-cell macrophage immuNKT-cell macrophageentimmunethaxisediates chasnic airway disease in a mouse model of Sendai virus infection (Kim et al., 2008).
It is striking that N66S in PB1-F2 is associated with increased virulence in a mouse model [57] but viruses having S at residue 66 of PB1-F2 arareand and were not present in the H9N2 viruses in this study.
In a mouse model of influenza virus-induced pneumonia, the overexpression of EC-SOD markedly ameliorated the inflammatory and oxidant responses in the lung [ 27].
In a recent study aimed at understanding the anti-inflammatory mechanism of MTX and its effect on acute viral induced arthritis, a mouse model of Ross River virus-induced inflammatory disease demonstrated that MTX treatment caused early onset of disease through increased monocyte production [ 22].
One previous study also showed effectiveness in vivo in a mouse model for West Nile virus using a nonphysiological hydrodymanic injection [18].
In a mouse model of Lymphocytic choriomeningitis virus (LCMV) infection wherein caspase-3 was also observed to be elevated during proliferative phases, it was suggested that pro-apoptotic mediators may function to degrade anti-apoptotic mediators and prepare cells for delayed apoptosis [38].
