Chaperonin CCT5 binding with porcine parvovirus NS1 promotes the interaction of NS1 and COPƐ to facilitate viral replication

Du, Qian; Zhang, Xuezhi; Xu, Ning; Ma, Mengyu; Miao, Bicheng; Huang, Yong; Tong, Dewen

doi:10.1016/j.vetmic.2022.109574

Cited by 3 publications

(2 citation statements)

References 27 publications

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“…PPV, the smallest and structurally simplest single-stranded linear DNA virus among animal viruses, is known to induce reproductive disorders in sows [13]. The dysregulation of proliferating trophoblast cells is closely associated with the occurrence and development of various reproductive disorders [14,15].…”

Section: Discussionmentioning

confidence: 99%

Porcine parvovirus infection induces necroptosis of porcine placental trophoblast cells via a ZBP1-mediated pathway

Xu,

Du,

Cheng

et al. 2024

Preprint

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Porcine parvovirus (PPV) infection induces germ cell death, leading to reproductive disorders in first-pregnant sows. Porcine placental trophoblast cells (PTCs) are the major target of PPV, and we have previously found that PPV infection leads to the death of PTCs by a non-apoptotic process, which may be related to PPV pathogenicity. The Z-nucleic acid-binding protein 1 (ZBP1) is often activated after virus invasion and mediates subsequent cell death. Here, we found that PPV infection induced ZBP1-mediated necroptosis of porcine PTCs in the presence of the apoptosis inhibitor, AC-DEVD-CHO. ZBP1 expression was upregulated during PPV infection, and ZBP1 knockout or RNA interference significantly reduced its expression along with the PPV-induced necroptosis. We discovered that RIPK3 and MLKL, but not Caspase-8, were involved in downstream signaling of ZBP1 during PPV infection; the phosphorylation levels of RIPK3 and MLKL were enhanced, but Caspase-8 was not significantly cleaved. The knockout of RIPK3 and MLKL significantly reduced the PPV infection-induced necroptosis of porcine PTCs. RIPK3 knockout did not affect the PPV infection-induced upregulation of ZBP1 expression, but blocked the activation of MLKL. MLKL knockout did not affect the upregulation of ZBP1 expression and RIPK3 phosphorylation during PPV infection. UV-inactivated PPV induced significantly less necroptosis of porcine PTCs than non-irradiated PPV. A PPV strain with a mutation in the translation initiation codon was still able to induce necroptosis of PTCs through the ZBP1/RIPK3/MLKL pathway. These results provide new insights into the pathogenic mechanism of PPV infection and suggest that PPV infection of porcine PTCs induces necroptosis through the viral DNA-dependent ZBP1/RIPK3/MLKL pathway.

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Section: Discussionmentioning

confidence: 99%

Porcine parvovirus infection induces necroptosis of porcine placental trophoblast cells via a ZBP1-mediated pathway

Xu,

Du,

Cheng

et al. 2024

Preprint

Self Cite

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“…Subsequent investigations revealed that to facilitate the connection of NS1/COPϵ, NS1 first interacts with the host protein CCT5 (149). In the process of PPV infection, it was also found that NS1 can mediate the complete and incomplete autophagy reaction of host cells to meet the needs of different viral replication periods (150). However, the molecular mechanism of interaction among parvovirus replication, DDR, and antiinfection immune cGAS-STING is unclear.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

For better or worse: crosstalk of parvovirus and host DNA damage response

Chen,

Liu,

Yang

et al. 2024

Front. Immunol.

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Parvoviruses are a group of non-enveloped DNA viruses that have a broad spectrum of natural infections, making them important in public health. NS1 is the largest and most complex non-structural protein in the parvovirus genome, which is indispensable in the life cycle of parvovirus and is closely related to viral replication, induction of host cell apoptosis, cycle arrest, DNA damage response (DDR), and other processes. Parvovirus activates and utilizes the DDR pathway to promote viral replication through NS1, thereby increasing pathogenicity to the host cells. Here, we review the latest progress of parvovirus in regulating host cell DDR during the parvovirus lifecycle and discuss the potential of cellular consequences of regulating the DDR pathway, targeting to provide the theoretical basis for further elucidation of the pathogenesis of parvovirus and development of new antiviral drugs.

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Knockout of the WD40 domain of ATG16L1 enhances foot and mouth disease virus replication

Wu,

Yang,

et al. 2024

BMC Genomics

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Chaperonin CCT5 binding with porcine parvovirus NS1 promotes the interaction of NS1 and COPƐ to facilitate viral replication

Cited by 3 publications

References 27 publications

Porcine parvovirus infection induces necroptosis of porcine placental trophoblast cells via a ZBP1-mediated pathway

Porcine parvovirus infection induces necroptosis of porcine placental trophoblast cells via a ZBP1-mediated pathway

For better or worse: crosstalk of parvovirus and host DNA damage response

Knockout of the WD40 domain of ATG16L1 enhances foot and mouth disease virus replication

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