Key result
Infection with both Coxsackievirus B3 Woodruff and GD strains activates the FoxO signaling pathway in HeLa cells, regulating downstream pathways including cell cycle, autophagy, and oxidative stress.
Why the study?
Coxsackievirus B3 is the major cause of viral myocarditis worldwide, but the precise pathogenic and disease mechanisms remain unclear.
Transcriptomic analysis reveals that Coxsackievirus B3 infection activates the FoxO signaling pathway in HeLa cells, providing insight into the pathogenic mechanisms of viral myocarditis.
Reveals candidate host genes for CVB3 interaction in vitro; leaves open their role in human myocarditis.
Coxsackievirus B3 (CVB3) is the major cause of viral myocarditis in human worldwide. Various studies have investigated the viral infection and pathogenic mechanisms. However, the precise disease mechanism is still not clear. In this study, RNA-seq technology was used to compare the transcriptomic profile of virus infected HeLa cells to the controls in order to analysis the key genes of host virus interaction. Two CVB3 strains, CVB3 Woodruff and GD16-69-CVB3 strain were selected to figure out the common disease mechanisms of both experimental and clinical strains respectively. Increased expression of cell cycle genes CCNG2, GADD45B, PIM1, RBM15, KLF10 and RIOK3, down regulation of CYBA were detected. Autophagy genes ATG12 and YOD1 were also upregulated during CVB3 infection. Slightly increase of SOD2 and ATG12 were shown in the expression of infected cells, meanwhile, little change was detected in GABARAP expression. Further, FoxO signaling pathway was enriched by KEGG analysis, shown a close interaction with the DEGs in the PPI network. Genes of related pathways such as cell cycle, autophagy and oxidative stress resistance were confirmed by RT-PCR as well. In conclusion, our results reveal that FoxO signaling pathway is a common mechanism activated during the infection of both CVB3 strains. And this pathway plays a regulatory role in downstream pathways such as cell cycle, autophagy, oxidative stress resistance and antiviral immune responds.
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Liu et al. (2021) studied Coxsackievirus B3 infection. Coxsackievirus B3 infection (Woodruff and GD strains) vs. Uninfected HeLa cells was evaluated on Differentially expressed genes and enriched signaling pathways. Infection with both Coxsackievirus B3 Woodruff and GD strains activates the FoxO signaling pathway in HeLa cells, regulating downstream pathways including cell cycle, autophagy, and oxidative stress.
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