Avian reovirus nonstructural protein p17-induced G(2)/M cell cycle arrest and host cellular protein translation shutoff involve activation of p53-dependent pathways.

The effects of avian reovirus (ARV) p17 protein on cell cycle progression and host cellular protein translation were studied. ARV infection and ARV p17 transfection resulted in the accumulation of infected and/or transfected cells in the G(2)/M phase of the cell cycle. The accumulation of cells in the G(2)/M phase was accompanied by upregulation and phosphorylation of the G(2)/M-phase proteins ATM, p53, p21(cip1/waf1), Cdc2, cyclin B1, Chk1, Chk2, and Cdc25C, suggesting that p17 induces a G(2)/M cell cycle arrest through activation of the ATM/p53/p21(cip1/waf1)/Cdc2/cyclin B1 and ATM/Chk1/Chk2/Cdc25C pathways.

Inhibitors of phosphatidylinositol 3-kinase and mTOR but not Akt enhance replication of bovine ephemeral fever virus.

Non-segmented, negative-sense RNA viruses (NNSVs) depend on Akt (protein kinase B) for efficient replication. Infection with bovine ephemeral fever virus (BEFV) increases Akt phosphorylation. This study examined the effect of inhibition of phosphatidylinositol 3-kinase (PI3K)-Akt signalling on BEFV replication, since PI3K is the major upstream regulator of Akt.

Baculovirus surface display of sigmaC and sigmaB proteins of avian reovirus and immunogenicity of the displayed proteins in a mouse model.

Avian reovirus (ARV), an important pathogen in poultry, causes arthritis, chronic respiratory disease, and malabsorption syndrome that cause considerable economic losses to the poultry industry. In present study, we have succeeded in construction of a universal baculovirus surface display system (UBSDS) that can display different foreign proteins on the envelope of baculovirus. Sequences encoding the signal peptide (SS), transmembrane domain (TM), and cytoplasmic domain (CTD) derived from the gp64 protein of baculovirus and histidine tag, respectively were inserted into the pBacCE vector.

Avian reovirus-induced apoptosis related to tissue injury.

Apoptosis plays an important role in pathogenesis of many viral infections. Infection of chicken with avian reovirus S1133 causes tissue injury related to virus-induced apoptosis. To determine whether avian reovirus (ARV) induced apoptosis in chicken tissues, six 3-week-old specific pathogen free White Leghorn chicks were inoculated with ARV S1133.

Apoptosis induction by avian reovirus through p53 and mitochondria-mediated pathway.

Although induction of apoptosis by avian reovirus has been demonstrated in primary chicken embryonic fibroblast and several cell lines, to date, the potential significance of avian reovirus (ARV)-induced apoptosis and its pathways in cultured cells are still largely unknown. We now provide the first evidence of upregulation of p53 and Bax and specifically for Bax translocation from cytosol to mitochondria following infection with a cytoplasmically replicating RNA virus. Bax translocation to the mitochondria led to the release of mitochondrial proapoptic factors cytochrome c and Smac/DIABLO from mitochondria to the cytosol, but not the release of apoptosis-inducting factor.

Development and characterization of monoclonal antibodies against avian reovirus sigma C protein and their application in detection of avian reovirus isolates.

Avian reovirus (ARV) is a non-enveloped virus with a segmented double-stranded RNA genome surrounded by a double icosahedral capsid shell. ARVs are associated with viral arthritis, immunosuppression, and enteric diseases in poultry. The sigma C protein was involved in induction of apoptosis and neutralization antibody.

Apoptosis induced by bovine ephemeral fever virus.

The potential significance of bovine ephemeral fever virus (BEFV)-induced apoptosis and involved viral molecules was fully unknown. In the present study, evidence is provided demonstrating that bovine ephemeral fever virus induces apoptosis in several cell lines. Five types of assays for apoptosis were used in examining BEFV-infected cells.

Rapid characterization of avian reoviruses using phylogenetic analysis, reverse transcription-polymerase chain reaction and restriction enzyme fragment length polymorphism.

A reverse transcription-polymerase chain reaction is described, which amplified the full-length sigmaC-encoding and sigmaNS-encoding genes of avian reovirus (ARV). DNA fragments of 1022 and 1152 base pairs were amplified among ARV isolates, respectively, indicating that there were no apparent deletions or insertions in these regions. Fragments amplified from vaccine strains and field isolates were digested with five different restriction enzymes Bcn I, Hae III, Taq I, Dde I, and Hinc II, respectively.

Avian reovirus sigmaC protein induces apoptosis in cultured cells.

The avian reovirus (ARV) infection is associated with various disease conditions in poultry. However, the pathogenesis mechanisms are poorly characterized. In the present study, we clearly demonstrated that the sigmaC of ARV S1133 strain induced apoptosis in both BHK-21 and Vero cells.

Detection of infectious bronchitis virus by multiplex polymerase chain reaction and sequence analysis.

A multiplex reverse transcription-polymerase chain reaction (RT-PCR) was developed to amplify the S1 and S2 genes of vaccine and recent Taiwanese isolates of infectious bronchitis virus (IBV). DNA fragments of 228 and 400 base pairs in length were amplified among IBV isolates in multiplex PCR, suggesting that there were no apparent deletions or insertions in these regions. No PCR products were amplified from unrelated avian viruses and negative controls.