Disease relevance of Reoviridae Infections

• These findings suggested that reovirus infection interfered with the progression of urethan-induced pulmonary adenoma rather than the induction of lung tumors by urethan [1].
• Dephosphorylation of eIF4E was not observed after Semliki Forest virus and reovirus infection [2].

Psychiatry related information on Reoviridae Infections

• Reovirus oncolysis: the Ras/RalGEF/p38 pathway dictates host cell permissiveness to reovirus infection [3].

High impact information on Reoviridae Infections

• Role of the S4 gene in the establishment of persistent reovirus infection in L cells [4].
• Effect of reovirus infection on pulmonary tumor response to urethan in strain A mice [1].
• We found that reovirus infection was blocked in the presence of the p38 inhibitor but not the JNK inhibitor [3].
• Cathepsin B Is Inhibited in Mutant Cells Selected during Persistent Reovirus Infection [5].
• Our results thus indicate that differences in susceptibility to cathepsin S-mediated sigma3 processing are responsible for strain differences in reovirus infection of macrophage-like P388D cells and other cathepsin S-expressing cells [6].

Chemical compound and disease context of Reoviridae Infections

• Herein we show that ribavirin inhibits reovirus-induced apoptosis in TRAIL-resistant HEK293 cells and prevents the ability of reovirus infection to sensitize TRAIL-resistant cells to TRAIL-induced apoptosis [7].
• No role for pepstatin-A-sensitive acidic proteinases in reovirus infections of L or MDCK cells [8].
• In the manganese study, neither reovirus infection nor dietary level had any effect on the incidence of leg abnormalities in male or female chickens [9].
• Reovirus infection significantly elevated the incidence of leg abnormalities in the biotin-, niacin-, and folic-acid-deficient chickens and decreased the incidence of leg abnormalities in choline-deficient chickens [9].

Biological context of Reoviridae Infections

• To investigate the role of CD8+, alpha/beta T-cell receptor (TCR)+ T cells in mucosal immunity to an enteric pathogen, we examined immune responses and viral clearance following enteric reovirus infection in C57BL/6, B6129F2, and beta2-microglobulin-deficient (beta2m-/-) mice [10].
• Plasmids expressing either the IGF-II pro-hormone or IGF-II without the carboxy terminal extension (E)-peptide sequence independently conferred high levels of cellular resistance to reovirus infection [11].

Anatomical context of Reoviridae Infections

• Expression of a beta1 integrin cDNA, along with a cDNA encoding JAM-A, in nonpermissive chicken embryo fibroblasts conferred susceptibility to reovirus infection [12].
• To directly assess the role of NE in reovirus infection of U937 cells, we examined viral growth in the presence of N-Ala-Ala-Pro-Val chloromethylketone, a NE-specific inhibitor [13].

Gene context of Reoviridae Infections

• To corroborate these findings, we introduced JAM-A or the structurally related JAM family members JAM-B and JAM-C into Chinese hamster ovary cells, which are poorly permissive for reovirus infection [14].
• Reovirus infection of the CNS enhances iNOS expression in areas of virus-induced injury [15].
• Mutant cells selected during persistent reovirus infection do not express mature cathepsin L and do not support reovirus disassembly [16].
• We propose that reovirus infection promotes apoptosis via the expression of DR5 and the release of TRAIL from infected cells [17].
• Reovirus infection activates JNK and the JNK-dependent transcription factor c-Jun [18].

References