Abstract
In this study, we found a much higher proportion of reticuloendotheliosis virus (REV) infected chicken embryo fibroblasts (CEF) were in active cell division phase than that of control cells which indicated that REV can affect the fate of CEF. So, we performed high-throughput sequencing and transcriptomic analysis to identify functional miRNAs, in order to figure out the possible mechanism in the interaction of REV with CEF. In total, 50 differentially expressed miRNAs (DEmiRNAs) were identified. Then target genes of DEmiRNAs were predicted and identified by transcriptome profile results. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment were conducted to analyze the identified target genes of miRNAs which showed that metabolism, cell cycle, and apoptosis were the most related pathways involved in infection of REV. We analyzed the genes related to cell cycle which indicated that CyclinD1-CDK6 complex played an important role in regulating the transition of the cell cycle from G1 phase to S phase during REV infection. Fluorescence microscope identification showed that REV inhibited the apoptosis of CEF which was in accordance with transcriptome results. A novel miRNA, named novel-72 was found, KEGG analysis was conducted to predict the biological function of its target genes which showed that those target genes were significantly enriched in mTOR signaling pathway and functioned to promote cell cycle and cell growth during the REV infection. In conclusion, REV could induce the up-regulation of cell metabolism, cell cycle and mTOR signaling pathway while inhibit apoptosis of the cell.
Highlights
Reticuloendotheliosis virus (REVs), as a member of the genus Gammaretrovirus in the family Retroviridae (Coffin, 1996), is a C-type avian retrovirus which can cause immunosuppression, runting disease, and lymphoma in a variety of avian hosts of chickens, turkeys, ducks, geese (Lin et al, 2009), peafowl, mallard (Jiang et al, 2014), and some other bird species (Barbacid et al, 1979; Bohls et al, 2006; Wang et al, 2012)
The polymerase chain reaction (PCR) products showed identical to the long terminal repeats (LTRs) region of REV (GenBank: AY842951.1), which indicate a successful establishment of REV infection model in VB cells
While 54.76% of the total REV infected cells were in cell cycle of G1 phase, 39.69% of them were in S phase, and 5.55% of them were in G2 phase (Figures 2, 3)
Summary
Reticuloendotheliosis virus (REVs), as a member of the genus Gammaretrovirus in the family Retroviridae (Coffin, 1996), is a C-type avian retrovirus which can cause immunosuppression, runting disease, and lymphoma in a variety of avian hosts of chickens, turkeys, ducks, geese (Lin et al, 2009), peafowl, mallard (Jiang et al, 2014), and some other bird species (Barbacid et al, 1979; Bohls et al, 2006; Wang et al, 2012). Functional miRNAs in REV Infection bird pathogens (Bao et al, 2015), an especially immunosuppressive virus such as Marek’s Disease Virus (MDV) (Dong et al, 2015) which cause dramatic damages to the poultry industry. The genome of REVT was confirmed to be derived from non-defective REV (Rice et al, 1982; Wilhelmsen et al, 1984), which includes LTRs, parts of the gag, pol, env genes, and an additional segment about 1.5 kb, termed v-rel (Chen and Temin, 1982; Stephens et al, 1983). Non-defective REV could induce lymphoma in its hosts. Lymphomas may cause death of its host and induce immunosuppression which increases its host susceptibility to concurrent or secondary bacterial or viral infections (Jiang et al, 2014). To date, the mechanisms of oncogenesis induced by REV remained to be elucidated
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