LiCl inhibits PRRSV infection by enhancing Wnt/β-catenin pathway and suppressing inflammatory responses

Hao, Haibo; Li, Wen; Li, Jiarong; Wang, Yue; Ni, Bo; Wang, Rui; Wang, Xin; Sun, Ming-Xia; Fan, Hongjie; Mao, Xiang

doi:10.1016/j.antiviral.2015.02.010

Cited by 53 publications

(40 citation statements)

References 72 publications

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“…3). Differences between our results, as well as the results obtained in the context of influenza virus (43) and PPRS virus (65), and the results of the work of Wang et al (62) could result from variations in the state of TBK1 in our respective cellular models. TBK1 is an enzyme whose activity strongly relies on its cellular localization, which can be affected by a wide diversity of mechanisms and signaling pathways, including not only pathogens but also cell growth and proliferation (66).…”

Section: Licl Treatment Enhances Constitutive Ifn-␤ Gene Expressioncontrasting

confidence: 99%

β-Catenin Upregulates the Constitutive and Virus-Induced Transcriptional Capacity of the Interferon Beta Promoter through T-Cell Factor Binding Sites

Marcato

Luron

Laqueuvre

et al. 2016

Molecular and Cellular Biology

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. Rapid upregulation of IFN-␤ gene expression occurs after recognition of viral nucleic acids by pattern recognition receptors (PRRs) consisting of either cytosolic receptors, such as retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated antigen 5 (MDA-5), or membrane-associated Toll-like receptors, such as Toll-like receptor 3 (TLR3) (3). After sensing single-or doublestranded RNA of viral origin, these receptors activate signaling pathways, implicating the phosphorylation and nuclear translocation of several transcription factors, among which is interferon regulatory factor 3 (IRF3), rapidly leading downstream to a robust activation of expression of the IFN-␤ gene. After being secreted, the IFN-␤ protein binds to the type I interferon receptor and triggers the JAK-STAT1/2 signal transduction pathway. This pathway leads to the activation and inhibition of the expression of a large set of genes that constitute the type I IFN response mounted to antagonize viral infection at different levels (4).Mice lacking IFN-␤ (5) or the subunit of the type I interferon receptor (6, 7) are highly susceptible to viral infections. They succumb to sublethal doses of a variety of viruses, thus confirming the main role of IFN-␤ in the establishment of an innate antiviral response. However, beyond the antiviral response, IFN-␤ affects a wide range of other biological functions; for the most part, these are related to modulation of the immune (innate and adaptive) and inflammatory responses as well as to cell proliferation and differentiation. Even though IFN-␤ has been described to have an anti-inflammatory benefit, it has also been implicated in the development of several inflammatory and autoimmune diseases (8-10). Hence, the beneficial or detrimental outcome of IFN-␤ expression for the organism depends on the timing and kinetics of IFN-␤ synthesis and the amount of IFN-␤ being synthesized (11,12). If a marked activation of IFN-␤ gene expression is required to efficiently set up the appropriate response to an external aggression, such as virus infection, this response needs to be adjusted in order to limit its pathological side effects.As expected for a gene with pleiotropic functions, its transcriptional state is regulated at different levels. At the cellular level, only a stochastic fraction of the infected cells produces 14) as a way to avoid an exacerbated and uncontrolled IFN response. At the nuclear level, one IFN-␤ allele localizes within interchromosomal regions rich in NF-B DNA binding sites before and after infection (15), whereas the other allele localizes next to pericentromeric heterochromatin (PCH) clusters in the absence of infection and dissociates from PCH clusters during infection (16). The monoallelic characteristic of these particular subnuclear localizations suggests that a yet undeciphered regulatory mechanism exists at the chromosome level. Finally, at the promoter level, the coordinated action of several transcription factors and chromatin-remodeling complexes (17-21) regulates the...

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Section: Licl Treatment Enhances Constitutive Ifn-␤ Gene Expressioncontrasting

confidence: 99%

β-Catenin Upregulates the Constitutive and Virus-Induced Transcriptional Capacity of the Interferon Beta Promoter through T-Cell Factor Binding Sites

Marcato

Luron

Laqueuvre

et al. 2016

Molecular and Cellular Biology

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“…Antiviral effects of LiCl have been extensively investigated. LiCl can inhibit the infection of some DNA and RNA viruses, such as herpes simplex virus (Skinner et al, 1980), canine parvovirus (Zhou et al, 2015), porcine parvovirus (Chen et al, 2015), pseudorabies herpesvirus (Sui et al, 2010), porcine reproductive and respiratory syndrome virus (Hao et al, 2015), feline calicivirus (Wu et al, 2015), infectious bronchitis virus, an avian coronavirus (Li et al, 2009) and transmissible gastroenteritis virus (TGEV), a porcine coronavirus (Ren et al, 2011). Both PEDV and TGEV are classified into group I of the genus Alphacoroavirus.…”

Section: Introductionmentioning

confidence: 99%

Antiviral effect of lithium chloride on porcine epidemic diarrhea virus in vitro

Gao

et al. 2018

Research in Veterinary Science

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Porcine epidemic diarrhea virus (PEDV), a member of the Coronaviridae family, causes acute diarrhea, vomiting, dehydration, and high mortality rates in neonatal piglets. Severe outbreaks of PEDV variants have re-emerged in Asia and North America since 2010, causing tremendous economic losses to the swine industry. The lack of effective therapeutic treatment promotes the research for new antivirals. Lithium chloride (LiCl) has been reported as a potential antiviral drug for certain viruses. In this study, the antiviral effect of LiCl on PEDV in Vero cells was evaluated. Real-time quantitative PCR and indirect immunofluorescence assay indicated that LiCl effectively inhibited the entry and replication of PEDV in Vero cells. The expression of viral RNA and protein of PEDV in Vero cells was suppressed in a dose-dependent manner by LiCl. Moreover, addition of LiCl inhibited both early and late cell apoptosis induced by PEDV. Our data implied that LiCl could be a potential antiviral drug against PEDV infection. Further studies are required to explore the antiviral effect of lithium chloride on PEDV infection in vivo.

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“…Lithium chloride (LiCl) is widely applied as an important therapeutic agent for nervous system disorders [15], including Alzheimer's disease [8], and for serous ovarian cancer [20] and diabetes [12]. Several studies have suggested that LiCl can act as an antiviral agent for inhibiting the growth of viruses, such as coronavirus [27], herpes simplex virus type 1 [29], porcine reproductive and respiratory syndrome virus (PRRSV) [11] and infectious bronchitis virus [13]. Moreover, LiCl can suppress host inflammatory responses [11], regulate cell apoptosis [27], and restore the synthesis of host proteins in virus-infected cells [43].…”

Section: Introductionmentioning

confidence: 99%

In vitro antiviral effect of germacrone on feline calicivirus

Liu

et al. 2016

Arch Virol

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Feline calicivirus (FCV) often causes respiratory tract and oral disease in cats and is a highly contagious virus. Widespread vaccination does not prevent the spread of FCV. Furthermore, the low fidelity of the RNA-dependent RNA polymerase of FCV leads to the emergence of new variants, some of which show increased virulence. Currently, few effective anti-FCV drugs are available. Here, we found that germacrone, one of the main constituents of volatile oil from rhizoma curcuma, was able to effectively reduce the growth of FCV strain F9 in vitro. This compound exhibited a strong anti-FCV effect mainly in the early phase of the viral life cycle. The antiviral effect depended on the concentration of the drug. In addition, germacrone treatment had a significant inhibitory effect against two other reference strains, 2280 and Bolin, and resulted in a significant reduction in the replication of strains WZ-1 and HRB-SS, which were recently isolated in China. This is the first report of antiviral effects of germacrone against a calicivirus, and extensive in vivo research is needed to evaluate this drug as an antiviral therapeutic agent for FCV.

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LiCl inhibits PRRSV infection by enhancing Wnt/β-catenin pathway and suppressing inflammatory responses

Cited by 53 publications

References 72 publications

β-Catenin Upregulates the Constitutive and Virus-Induced Transcriptional Capacity of the Interferon Beta Promoter through T-Cell Factor Binding Sites

β-Catenin Upregulates the Constitutive and Virus-Induced Transcriptional Capacity of the Interferon Beta Promoter through T-Cell Factor Binding Sites

Antiviral effect of lithium chloride on porcine epidemic diarrhea virus in vitro

In vitro antiviral effect of germacrone on feline calicivirus

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