Litcius/Paper detail

Swine acute diarrhea syndrome coronavirus-induced apoptosis is caspase- and cyclophilin D- dependent

Jiyu Zhang, Yuru Han, Hongyan Shi, Jianfei Chen, Xin Zhang, Xiaobo Wang, Ling Zhou, Jianbo Liu, Jialin Zhang, Zhaoyang Ji, Zhaoyang Jing, Jingyun Ma, Da Shi, Li Feng

2020Emerging Microbes & Infections59 citationsDOIOpen Access PDF

Abstract

. The use of a pan-caspase inhibitor resulted in the inhibition of SADS-CoV-induced apoptosis and reduction in SADS-CoV replication, suggestive of the association of a caspase-dependent pathway. Furthermore, SADS-CoV infection activated the initiators caspase-8 and -9 and upregulated FasL and Bid cleavage, demonstrating a crosstalk between the extrinsic and intrinsic pathways. However, the proapoptotic proteins Bax and Cytochrome c (Cyt c) relocalized to the mitochondria and cytoplasm, respectively, after infection by SADS-CoV. Moreover, Vero E6 and IPI-2I cells treated with cyclosporin A (CsA), an inhibitor of mitochondrial permeability transition pore (MPTP) opening, were completely protected from SADS-CoV-induced apoptosis and viral replication, suggesting the involvement of cyclophilin D (CypD) in these processes. Altogether, our results indicate that caspase-dependent FasL (extrinsic)- and mitochondria (intrinsic)- mediated apoptotic pathways play a central role in SADS-CoV-induced apoptosis that facilitates viral replication. In summary, these findings demonstrate mechanisms by which SADS-CoV induces apoptosis and improve our understanding of SADS-CoV pathogenesis.

Topics & Concepts

ApoptosisBiologyMitochondrionCaspaseViral replicationVero cellIntrinsic apoptosisCell biologyCytochrome cCaspase 8Programmed cell deathCoronavirusCaspase 3Mitochondrial permeability transition poreVirologyVirusMedicineBiochemistryCoronavirus disease 2019 (COVID-19)Infectious disease (medical specialty)DiseasePathologySARS-CoV-2 and COVID-19 ResearchCell death mechanisms and regulationAnimal Virus Infections Studies