Cholesterol 25-hydroxylase inhibits encephalomyocarditis virus replication through enzyme activity-dependent and independent mechanisms

Li, Shihai; Li, Liang; Zhu, Huixin; Shi, Mengyu; Fan, Huiying; Gao, Yanni; Wang, Xianwei; Jiang, Ping; Bai, Juan

doi:10.1016/j.vetmic.2020.108658

Cited by 13 publications

(13 citation statements)

References 35 publications

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“…This oxysterol was hampering the in vitro replication of another coronavirus, namely the porcine transmissible gastroenteritis virus (TGEV) [ 103 ]. Still with regard to the enzyme CH25H, its knock-out was shown to lose the ability of inhibiting in vitro replication of the encephalomyocarditis virus (EMCV) [ 104 ]. Moreover, the 25OHC treatment of piglets challenged with the Porcine reproductive and respiratory syndrome (PRRS) virus, which induces a severe respiratory failure in infected pigs, provided a significant reduction of the necrotic and inflammatory lesions of the lungs, so that the clinical symptoms of the syndrome resulted to be mild [ 105 ].…”

Section: Pharma Industry: Oxysterols As Pharmaceutical Drugsmentioning

confidence: 99%

Oxysterols: From redox bench to industry

et al. 2022

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More and more attention is nowadays given to the possible translational application of a great number of biochemical and biological findings with the involved molecules. This is also the case of cholesterol oxidation products, redox molecules over the last years deeply investigated for their implication in human pathophysiology. Oxysterols of non-enzymatic origin, the excessive increase of which in biological fluids and tissues is of toxicological relevance for their marked pro-oxidant and pro-inflammatory properties, are increasingly applied in clinical biochemistry as molecular markers in the diagnosis and monitoring of several human and veterinary diseases. Conversely, oxysterols of enzymatic origin, the production of which is commonly under physiological regulation, could be considered and tested as promising pharmaceutical agents because of their antiviral, pro-osteogenic and antiadipogenic properties of some of them. Very recently, the quantification of oxysterols of non-enzymatic origin has been adopted in a systematic way to evaluate, monitor and improve the quality of cholesterol-based food ingredients, that are prone to auto-oxidation, as well as their industrial processing and the packaging and the shelf life of the finished food products. The growing translational value of oxysterols is here reviewed in its present and upcoming applications in various industrial fields.

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Section: Pharma Industry: Oxysterols As Pharmaceutical Drugsmentioning

confidence: 99%

Oxysterols: From redox bench to industry

et al. 2022

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“…Coronavirus infection induces host cells to alter the expression of certain cholesterol metabolizing enzymes and metabolites which may exert antiviral effects ( Figure 2A ) ( 77 ). Indeed, both 25-hydroxycholesterol (25HC) and 27-hydroxycholesterol (27HC) are physiologically produced by the enzymatic oxidation of cholesterol and may be used to inhibit enveloped and non-enveloped human viruses ( 183 , 184 ) and highly pathogenic viruses, including Zika ( 185 ), mammalian reovirus ( 186 ), Lassa virus ( 187 ), encephalomyocarditis virus ( 188 ), porcine reproductive and respiratory syndrome virus ( 189 ). A recent study reported that the 25HC treatment of mice infected with SARS-CoV-2 significantly reduced virus numbers in the lungs and trachea ( 148 ).…”

Section: The Role Of Cholesterol Metabolism During the Coronavirus Li...mentioning

confidence: 99%

Coronavirus Infection and Cholesterol Metabolism

et al. 2022

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Host cholesterol metabolism remodeling is significantly associated with the spread of human pathogenic coronaviruses, suggesting virus-host relationships could be affected by cholesterol-modifying drugs. Cholesterol has an important role in coronavirus entry, membrane fusion, and pathological syncytia formation, therefore cholesterol metabolic mechanisms may be promising drug targets for coronavirus infections. Moreover, cholesterol and its metabolizing enzymes or corresponding natural products exert antiviral effects which are closely associated with individual viral steps during coronavirus replication. Furthermore, the coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 infections are associated with clinically significant low cholesterol levels, suggesting cholesterol could function as a potential marker for monitoring viral infection status. Therefore, weaponizing cholesterol dysregulation against viral infection could be an effective antiviral strategy. In this review, we comprehensively review the literature to clarify how coronaviruses exploit host cholesterol metabolism to accommodate viral replication requirements and interfere with host immune responses. We also focus on targeting cholesterol homeostasis to interfere with critical steps during coronavirus infection.

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“…25HC broadly inhibits enveloped viruses by blocking virus entry (Liu et al, 2013). For some viruses, including PRRSV, CH25H could inhibit viral replication through enzyme activity-dependent and independent mechanisms (Lv et al, 2019;Li et al, 2020). CH25H restricts PRRSV replication by inhibiting virus entry and degrading Nsp1α via the ubiquitin-proteasome pathway with K169 in the Nsp1 protein serving as the main ubiquitination location .…”

Section: Cholesterol 25-hydroxylase (Ch25h)mentioning

confidence: 99%

Evasion of Antiviral Innate Immunity by Porcine Reproductive and Respiratory Syndrome Virus

et al. 2021

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Innate immunity is the front line for antiviral immune responses and bridges adaptive immunity against viral infections. However, various viruses have evolved many strategies to evade host innate immunity. A typical virus is the porcine reproductive and respiratory syndrome virus (PRRSV), one of the most globally devastating viruses threatening the swine industry worldwide. PRRSV engages several strategies to evade the porcine innate immune responses. This review focus on the underlying mechanisms employed by PRRSV to evade pattern recognition receptors signaling pathways, type I interferon (IFN-α/β) receptor (IFNAR)-JAK-STAT signaling pathway, and interferon-stimulated genes. Deciphering the antiviral immune evasion mechanisms by PRRSV will enhance our understanding of PRRSV’s pathogenesis and help us to develop more effective methods to control and eliminate PRRSV.

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Cholesterol 25-hydroxylase inhibits encephalomyocarditis virus replication through enzyme activity-dependent and independent mechanisms

Cited by 13 publications

References 35 publications

Oxysterols: From redox bench to industry

Oxysterols: From redox bench to industry

Coronavirus Infection and Cholesterol Metabolism

Evasion of Antiviral Innate Immunity by Porcine Reproductive and Respiratory Syndrome Virus

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