Research advances on interferon (IFN) response during BVDV infection

Song, Quanjiang; Zhao, Xin; Cao, Changchang; Duan, Mingmei; Shao, Chunyan; Jiang, Sheng; Zeng, Bin; Zhou, Yingshan; Dong, Wanyu; Yang, Yang; Wang, Xiaodu; Song, Houhui

doi:10.1016/j.rvsc.2022.04.011

Cited by 6 publications

(4 citation statements)

References 113 publications

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“…Previous studies have shown the critical role of IFN-I in resistance to BVDV replication [ 25 , 26 ]. The effect of CALCOCO2 on IFN-β and ISG production in CALCOCO2-overexpressing stable cell lines during BVDV infection (MOI = 0.1 or 5) was first examined.…”

Section: Resultsmentioning

confidence: 99%

The host protein CALCOCO2 interacts with bovine viral diarrhoea virus Npro, inhibiting type I interferon production and thereby promoting viral replication

Wang,

Wei,

et al. 2023

Virulence

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Bovine viral diarrhoea-mucosal disease caused by bovine viral diarrhoea virus (BVDV) is a major infectious disease that affects the cattle industry. The nonstructural protein Npro of BVDV antagonizes the type I interferon (IFN-I) pathway, thereby escaping the host immune response. The exact mechanism by which Npro uses host proteins to inhibit IFN-I production is unclear. The host protein CALCOCO2 was identified as a binding partner of Npro using a yeast two-hybrid screen. The interaction between Npro and CALCOCO2 was confirmed by yeast co-transformation, co-immunoprecipitation assays, and GST pull-down assays. The stable overexpression of CALCOCO2 markedly promoted BVDV propagation, while the knockdown of CALCOCO2 significantly inhibited BVDV replication in MDBK cells. Interestingly, CALCOCO2 inhibited IFN-I and IFN-stimulated gene production in BVDV-infected cells. Ectopic expression of CALCOCO2 effectively reduced IRF3 protein levels via the proteasome pathway. CALCOCO2 was found to promote Npro-mediated ubiquitination degradation of IRF3 by interacting with IRF3. Our results demonstrate the molecular mechanism by which Npro recruits the CALCOCO2 protein to regulate IRF3 degradation to inhibit IFN-I production.

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Section: Resultsmentioning

confidence: 99%

The host protein CALCOCO2 interacts with bovine viral diarrhoea virus Npro, inhibiting type I interferon production and thereby promoting viral replication

Wang,

Wei,

et al. 2023

Virulence

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“…However, NCP/CP BVDV N pro could not prevent the activation of NF-kB by poly(I:C) (Hilton et al, 2006). Intriguingly, although the IFN-I induced by BVDV was suppressed by viral proteins, NCP BVDV and CP BVDV could still produce a certain amount of IFNs after infecting pDC, and the total IFNs generated by CP BVDV was observably higher than that of NCP BVDV (Lee et al, 2008;Reid et al, 2016;Song et al, 2022). When investigating the reasons for this phenomenon, researchers found that NCP BVDV infection did not cause the activation of NF-kB, while CP BVDV could induce NF-kB activation (Gil et al, 2006b;Maldonado et al, 2020).…”

Section: Strategies For Pestiviruses To Circumvent Interferonsmentioning

confidence: 92%

Pestiviruses infection: Interferon-virus mutual regulation

Hong

Yang²,

Wang³

et al. 2023

Front. Cell. Infect. Microbiol.

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Pestiviruses are a class of viruses that in some cases can cause persistent infection of the host, thus posing a threat to the livestock industry. Interferons (IFNs) are a group of secreted proteins that play a crucial role in antiviral defense. In this review, on the one hand, we elaborate on how pestiviruses are recognized by the host retinoic acid-inducible gene-I (RIG-I), melanoma-differentiation-associated protein 5 (MDA5), and Toll-like receptor 3 (TLR3) proteins to induce the synthesis of IFNs. On the other hand, we focus on reviewing how pestiviruses antagonize the production of IFNs utilizing various strategies mediated by self-encoded proteins, such as the structural envelope protein (Erns) and non-structural protein (Npro). Hence, the IFN signal transduction pathway induced by pestiviruses infection and the process of pestiviruses blockade on the production of IFNs intertwines into an intricate regulatory network. By reviewing the interaction between IFN and pestiviruses (based on studies on BVDV and CSFV), we expect to provide a theoretical basis and reference for a better understanding of the mechanisms of induction and evasion of the innate immune response during infection with these viruses.

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“…To classify BVDV, scientists observe its effects on cell cultures, categorizing it as cytopathic (CP) or noncytopathic (NCP) [ 16 , 17 , 18 , 19 , 20 ]. BVDV can be classified into three genotypes, namely, genotype 1 (BVDV-1), genotype 2 (BVDV-2), and genotype 3 (BVDV-3), based on the genetic variations in the viral genome [ 21 , 22 ].…”

Section: Bovine Viral Diarrhea Virus and Its Induced Immunosuppressionmentioning

confidence: 99%

New Insights into the Role and Therapeutic Potential of Heat Shock Protein 70 in Bovine Viral Diarrhea Virus Infection

Chen,

Bai,

Wang

et al. 2023

Microorganisms

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Bovine viral diarrhea virus (BVDV), a positive-strand RNA virus of the genus Pestivirus in the Flaviviridae family, is the causative agent of bovine viral diarrhea–mucosal disease (BVD-MD). BVDV’s unique virion structure, genome, and replication mechanism in the Flaviviridae family render it a useful alternative model for evaluating the effectiveness of antiviral drugs used against the hepatitis C virus (HCV). As one of the most abundant and typical heat shock proteins, HSP70 plays an important role in viral infection caused by the family Flaviviridae and is considered a logical target of viral regulation in the context of immune escape. However, the mechanism of HSP70 in BVDV infection and the latest insights have not been reported in sufficient detail. In this review, we focus on the role and mechanisms of HSP70 in BVDV-infected animals/cells to further explore the possibility of targeting this protein for antiviral therapy during viral infection.

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Research advances on interferon (IFN) response during BVDV infection

Cited by 6 publications

References 113 publications

The host protein CALCOCO2 interacts with bovine viral diarrhoea virus Npro, inhibiting type I interferon production and thereby promoting viral replication

The host protein CALCOCO2 interacts with bovine viral diarrhoea virus Npro, inhibiting type I interferon production and thereby promoting viral replication

Pestiviruses infection: Interferon-virus mutual regulation

New Insights into the Role and Therapeutic Potential of Heat Shock Protein 70 in Bovine Viral Diarrhea Virus Infection

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