DNAJA3 Interacts with PEDV S1 Protein and Inhibits Virus Replication by Affecting Virus Adsorption to Host Cells

Porcine epidemic diarrhea virus (PEDV) infection causes huge economic losses to the pig industry worldwide. DNAJA3, a member of the Hsp40 family proteins, is known to play an important role in the replication of several viruses. However, it remains unknown if it interacts with PEDV. We found that DN...

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Bibliographic Details
Published in:Viruses 2022-10, Vol.14 (11), p.2413
Main Authors: Zheng, Jingyou, Gao, Qin, Xu, Jidong, Xu, Xiaohan, Shan, Ying, Shi, Fushan, Yue, Min, He, Fang, Fang, Weihuan, Li, Xiaoliang
Format: Article
Language:English
Subjects:
Adsorption
Animals
Antibiotics
Antibodies
Antiviral activity
Apoptosis
Chlorocebus aethiops
Cloning
Coronavirus Infections
Coronaviruses
Diarrhea
Diseases
DNAJA3
Gene silencing
Genetic aspects
Genomes
Heat shock proteins
Hsp40 protein
Laboratories
Physiological aspects
Plasmids
porcine epidemic diarrhea virus
Porcine epidemic diarrhea virus - genetics
Proteins - pharmacology
Replication
spike protein S1
Swine
Transmissible gastroenteritis
Vero Cells
viral adsorption
Virus Replication
Viruses
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Summary:Porcine epidemic diarrhea virus (PEDV) infection causes huge economic losses to the pig industry worldwide. DNAJA3, a member of the Hsp40 family proteins, is known to play an important role in the replication of several viruses. However, it remains unknown if it interacts with PEDV. We found that DNAJA3 interacted with PEDV S1, initially with yeast two-hybrid screening and later with Co-IP, GST pull-down, and confocal imaging. Further experiments showed the functional relationship between DNAJA3 and PEDV in the infected IPEC-J2 cells. DNAJA3 overexpression significantly inhibited PEDV replication while its knockdown had the opposite effect, suggesting that it is a negative regulator of PEDV replication. In addition, DNAJA3 expression could be downregulated by PEDV infection possibly as the viral strategy to evade the suppressive role of DNAJA3. By gene silencing and overexpression, we were able to show that DNAJA3 inhibited PEDV adsorption to IPEC-J2 cells but did not affect virus invasion. In conclusion, our study provides clear evidence that DNAJA3 mediates PEDV adsorption to host cells and plays an antiviral role in IPEC-J2 cells.
ISSN:1999-4915
1999-4915
DOI:10.3390/v14112413