Duck hepatitis A virus type 1 mediates cell cycle arrest in the S phase

Author:

Liu Yuanzhi,Li Yanglin,Wang Mingshu,Cheng AnchunORCID,Ou Xumin,Mao Sai,Sun Di,Wu Ying,Yang Qiao,Jia Renyong,Tian Bin,Zhang Shaqiu,Zhu Dekang,Chen Shun,Liu Mafeng,Zhao Xinxin,Huang Juan,Gao Qun,Yu Yanling,Zhang Ling

Abstract

Abstract Background Duck hepatitis A virus type 1 (DHAV-1) is one of the most serious pathogens endangering the duck industry. However, there are few studies on the regulation of the cell cycle by DHAV-1. Methods In this study, flow cytometry was applied to analyze the effect of DHAV-1 infection on the cell cycle of duck embryo fibroblasts (DEFs). Subsequently, we analyzed the effects of cell cycle phases on DHAV-1 replication by real-time reverse transcriptase quantitative PCR (real-time RT-qPCR). Results Flow cytometry data analysis found that DEFs in the S phase increased by 25.85% and 54.21% at 24 h and 48 h after DHAV-1 infection, respectively. The levels of viral RNA detected by real-time RT-qPCR were higher in the DEFs with synchronization in the S phase or G0/G1 phase than in the control group. However, there was no difference in viral copy number between the G2/M phase arrest and control groups. In addition, non-structural protein 3D of DHAV-1 significantly increased cells in the S phase, indicating that 3D protein is one of the reasons for the cell cycle arrest in the S phase. Conclusions In summary, DHAV-1 infection induces the cell cycle arrest of DEFs in the S phase. Both S phase and G0/G1 phase synchronization facilitate the replication of DHAV-1, and 3D protein is one of the reasons for the S phase arrest.

Funder

China Agriculture Research System of MOF and MARA, Sichuan Veterinary Medicine and Drug Innovation Group of China Agricultural Research System

Publisher

Springer Science and Business Media LLC

Subject

Infectious Diseases,Virology

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