Duck Hepatitis A Virus Type 1 Mediates Cell Cycle Arrest in the S Phase

Overview

Journal Virol J

Publisher Biomed Central

Specialty Microbiology

Date 2022 Jun 27

PMID 35761382

Authors

Yuanzhi Liu

Yanglin Li

Mingshu Wang

Anchun Cheng

Xumin Ou

Sai Mao

Di Sun

Ying Wu

Qiao Yang

Renyong Jia

Bin Tian

Shaqiu Zhang

Dekang Zhu

Shun Chen

Mafeng Liu

Xinxin Zhao

Juan Huang

Qun Gao

Yanling Yu

Ling Zhang

Affiliations

Soon will be listed here.

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.

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