A critical role for MSR1 in vesicular stomatitis virus infection of the central nervous system

Yang, Duomeng; Lin, Tao; Harrison, Andrew G.; Geng, Tingting; Wang, Penghua

doi:10.1016/j.isci.2021.102678

Cited by 5 publications

(3 citation statements)

References 52 publications

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“…Mice lacking MSR1 displayed significantly decreased mortality and morbidity, with MSR1 being shown to have a significant impact on VSV infection in the central nervous system. Cellular entry of VSV was dependent on MSR1 functioning as a co-receptor for low density lipoprotein receptor (LDLR) mediated uptake ( 133 ).…”

Section: Response To Pathogensmentioning

confidence: 99%

The role of macrophage scavenger receptor 1 (MSR1) in inflammatory disorders and cancer

Gudgeon

Marín-Rubio²,

Trost³

2022

Front. Immunol.

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Macrophage scavenger receptor 1 (MSR1), also named CD204, holds key inflammatory roles in multiple pathophysiologic processes. Present primarily on the surface of various types of macrophage, this receptor variably affects processes such as atherosclerosis, innate and adaptive immunity, lung and liver disease, and more recently, cancer. As highlighted throughout this review, the role of MSR1 is often dichotomous, being either host protective or detrimental to the pathogenesis of disease. We will discuss the role of MSR1 in health and disease with a focus on the molecular mechanisms influencing MSR1 expression, how altered expression affects disease process and macrophage function, the limited cell signalling pathways discovered thus far, the emerging role of MSR1 in tumour associated macrophages as well as the therapeutic potential of targeting MSR1.

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Section: Response To Pathogensmentioning

confidence: 99%

The role of macrophage scavenger receptor 1 (MSR1) in inflammatory disorders and cancer

Gudgeon

Marín-Rubio²,

Trost³

2022

Front. Immunol.

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“…VSV also invades the central nervous system through the peripheral nerves to cause paralytic symptoms. [32,33] In addition, a remarkably tractable vector was found in the VSV, enabling it to work for genetic manipulation and stimulating the immune system. Currently, there is no effective specific treatment for VSV infections.…”

Section: Discussionmentioning

confidence: 99%

Dietary Flavonoid Quercetin Supplement Promotes Antiviral Innate Responses Against Vesicular Stomatitis Virus Infection by Reshaping the Bacteriome and Host Metabolome in Mice

Li,

Zhu,

et al. 2024

Molecular Nutrition Food Res

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ScopeActive ingredients in functional foods exhibit broad‐spectrum antiviral activity. The objective of this study is to investigate the protective effect of quercetin derived from bee propolis, a natural product with antiviral activity and modulating effects on the gut microbiota, against vesicular stomatitis virus (VSV) infection.Methods and resultsThrough a cellular‐based study, this study demonstrates that quercetin can modulate the activity of interferon‐regulating factor 3 (IRF3). In vivo, it shows that quercetin protects mice from VSV infection by enhancing interferon production and inhibiting the production of proinflammatory cytokines. The study conducts 16S rRNA‐based gut microbiota and nontargets metabolomics analyses to elucidate the mechanisms underlying quercetin‐mediated bidirectional communication between the gut microbiome and host metabolome during viral infection. Quercetin not only ameliorates VSV‐induced dysbiosis of the intestinal flora but also alters serum metabolites related to lipid metabolism. Cross‐correlations between the gut bacteriome and the serum metabolome indicate that quercetin can modulate phosphatidylcholine (16:0/0:0) and 5‐acetylamino‐6‐formylamino‐3‐methyluracil to prevent VSV infection.ConclusionThis study systematically elucidates the anti‐VSV mechanism of quercetin through gut bacteriome and host metabolome assays, offering new insights into VSV treatment and revealing the mechanisms behind a novel disease management strategy using dietary flavonoid supplements.

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“…EMCV, VSV infection and disease score in mice was performed according to previous methods 16,48 . Virus stock was diluted properly in sterile phosphate-buffered saline (PBS).…”

Section: Viral Infection In Micementioning

confidence: 99%

UBR5 promotes antiviral immunity by disengaging the transcriptional brake on RIG-I like receptors

Yang,

Geng,

Harrison

et al. 2024

Nat Commun

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The Retinoic acid-Inducible Gene I (RIG-I) like receptors (RLRs) are the major viral RNA sensors essential for the initiation of antiviral immune responses. RLRs are subjected to stringent transcriptional and posttranslational regulations, of which ubiquitination is one of the most important. However, the role of ubiquitination in RLR transcription is unknown. Here, we screen 375 definite ubiquitin ligase knockout cell lines and identify Ubiquitin Protein Ligase E3 Component N-Recognin 5 (UBR5) as a positive regulator of RLR transcription. UBR5 deficiency reduces antiviral immune responses to RNA viruses, while increases viral replication in primary cells and mice. Ubr5 knockout mice are more susceptible to lethal RNA virus infection than wild type littermates. Mechanistically, UBR5 mediates the Lysine 63-linked ubiquitination of Tripartite Motif Protein 28 (TRIM28), an epigenetic repressor of RLRs. This modification prevents intramolecular SUMOylation of TRIM28, thus disengages the TRIM28-imposed brake on RLR transcription. In sum, UBR5 enables rapid upregulation of RLR expression to boost antiviral immune responses by ubiquitinating and de-SUMOylating TRIM28.

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A critical role for MSR1 in vesicular stomatitis virus infection of the central nervous system

Cited by 5 publications

References 52 publications

The role of macrophage scavenger receptor 1 (MSR1) in inflammatory disorders and cancer

The role of macrophage scavenger receptor 1 (MSR1) in inflammatory disorders and cancer

Dietary Flavonoid Quercetin Supplement Promotes Antiviral Innate Responses Against Vesicular Stomatitis Virus Infection by Reshaping the Bacteriome and Host Metabolome in Mice

UBR5 promotes antiviral immunity by disengaging the transcriptional brake on RIG-I like receptors

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