Molecular biology of adenovirus type 2 semipermissive infections I. Viral growth and expression of viral replicative functions during restricted adenovirus infection
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Cited by (36)
IIIa deleted adenovirus as a single-cycle genome replicating vector
2014, VirologyCitation Excerpt :It is unclear exactly why expression declined in mouse cells; however, this may be due to defects in the ability of human adenoviruses to complete the viral life cycle after genome replication. In particular, human Ads may fail to express late capsid components which may contribute to instability of newly synthesized viral genomes (Eggerding and Pierce, 1986). It is also possible that reduce late gene expression in mouse cells may perturb mouse cells and not humans cells to reduce expression.
Adenovirus type 35, but not type 5, stimulates NK cell activation via plasmacytoid dendritic cells and TLR9 signaling
2012, Molecular ImmunologyCitation Excerpt :In mice, IFN I and dendritic cell-dependent activation of NK cells has been implicated in the clearance of cells infected with adenoviral vectors (Zhu et al., 2008, 2010). However, since human adenovirus is known to result in only low yields of productive virus after infection of murine cells due to limited viral replication, imperfect protein synthesis and an abortive virus life cycle, mouse models are not optimal for studying immune responses to human adenovirus (Duncan et al., 1978; Eggerding and Pierce, 1986; Ganly et al., 2000; Ginsberg et al., 1991). After infection with recombinant adenoviral vectors, human fibroblasts were more susceptible to lysis by NK cells in association with the NK cell-activating receptor NKG2D (Tomasec et al., 2007).
Establishment of a mammary carcinoma cell line from Syrian hamsters treated with N-methyl-N-nitrosourea
2011, Cancer LettersCitation Excerpt :Thus, a more realistic animal model that is permissive or at least semi-permissive for human adenovirus replication would be of great value to the field of adenovirus-based cancer therapy. In contrast to most other species examined, the Syrian hamster is permissive for human adenovirus replication [29–31]. The adenovirus is able to infect, replicate, and spread from cell to cell in vitro in cell lines derived from this animal, and replicates in vivo in the lungs, liver, and other organs [11].
Active adenoviral vascular penetration by targeted formation of heterocellular endothelial-epithelial syncytia
2011, Molecular TherapyCitation Excerpt :As the Pit-1 receptor required for GALV-mediated fusion is absent on murine cells,10 any host stromal cells such as pericytes and fibroblasts within the xenograft will create a barrier to limit the interaction of infected endothelial cells with the HEK 293 cells. Another possible factor limiting the efficiency of this model system is the abortive or poor replication efficiency of human Ads in mouse cells29,30,31 due to repression of viral E1A enhancer activity32 and defects in the synthesis of structural proteins.33 Such repression could still occur to some extent despite the E1 gene products being provided in trans by the HEK 293 component of the syncytium.
Novel immunocompetent murine tumor models for the assessment of replication-competent oncolytic adenovirus efficacy
2003, Molecular TherapyCitation Excerpt :To date, all published animal tumor model efficacy data with replication-selective adenoviruses has come from immunodeficient mouse–human tumor xenograft models [28–30]. This focus on human tumor xenografts was in part due to data from decades earlier demonstrating that normal murine tissues (e.g., lung, fibroblasts) were not permissive for adenoviral replication [31–33]. For example, intranasal adenovirus administration led to viral DNA replication and associated tissue toxicities, but virus titers were several orders of magnitude less than the input dose.
"Man's best friend": A new model system for cancer therapeutics?
2003, Molecular Therapy