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Published on: September 25, 2019
Duck hepatitis A virus type 1 mediates cell cycle arrest in the S phase
Yuanzhi Liu1,2,3, Yanglin Li1,2,3, Mingshu Wang1,2,3
1Institute of Preventive Veterinary Medicine, Sichuan Agricultural University, Wenjiang, Chengdu City, 611130, Sichuan, China.
Duck hepatitis A virus type 1 (DHAV-1) causes cell cycle arrest in duck embryo fibroblasts (DEFs). DHAV-1 replication is enhanced in S and G0/G1 phases, with protein 3D contributing to S phase arrest.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Duck hepatitis A virus type 1 (DHAV-1) poses a significant threat to the duck industry.
- Limited research exists on DHAV-1's impact on host cell cycle regulation.
Purpose of the Study:
- To investigate the effects of DHAV-1 infection on the cell cycle of duck embryo fibroblasts (DEFs).
- To determine how different cell cycle phases influence DHAV-1 replication.
Main Methods:
- Utilized flow cytometry to analyze cell cycle distribution in DHAV-1 infected DEFs.
- Employed real-time reverse transcriptase quantitative PCR (real-time RT-qPCR) to quantify viral RNA levels across cell cycle phases.
Main Results:
- DHAV-1 infection led to a significant increase in DEFs entering the S phase (25.85% at 24h, 54.21% at 48h).
- Viral RNA levels were elevated in DEFs synchronized in the S or G0/G1 phases compared to controls.
- DHAV-1 non-structural protein 3D was identified as a factor inducing S phase arrest.
Conclusions:
- DHAV-1 infection causes S phase cell cycle arrest in DEFs.
- S and G0/G1 phase synchronization promotes DHAV-1 replication.
- DHAV-1 protein 3D contributes to S phase arrest, impacting viral replication.
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