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Antibiotics driven gut microbiome perturbation alters the immune response to the rabies vaccine

ABSTRACT: Antibiotics driven gut microbiome perturbation alters the immune response to the rabies vaccine

PROVIDER: PRJNA1249091 | ENA |

REPOSITORIES: ENA

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Antibiotics driven gut microbiome perturbation alters the immune response to the rabies vaccine

Project description:The gut microbiome plays a crucial role in modulating human immunity. Previously, we found that antibiotic-induced microbiome perturbation affected influenza vaccine responses depending on pre-existing immunity levels. However, its impact on primary responses remains unclear. Here, we employed a systems biology approach to analyze the impact of antibiotic administration on primary and secondary immune responses to the rabies vaccine in humans. Antibiotic administration disrupted the microbiome, reducing gut bacterial load and causing long-lasting reduction in commensal diversity. This alteration was associated with reduced rabies-specific humoral responses. Multi-omics profiling revealed that antibiotic administration induced: 1) an enhanced pro-inflammatory signature early after vaccination, 2) a shift in the balance of vaccine-specific T-helper 1(Th1) to T-follicular-helper response towards Th1 phenotype, 3) profound alterations in metabolites, particularly in secondary bile acids in blood. By integrating multi-omics datasets, we generated a multi-scale, multi-response network that revealed key regulatory nodes including the microbiota, secondary bile acids, and humoral immunity to vaccination.

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Project description:Analyses of viruses from vaccine induced rabies cases and corresponding vaccine batches

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LncRNA RVRL1 restricts rabies virus infection by disrupting PRC2 complex [ChIP-seq]

Project description:Rabies is an ancient infectious disease but still lacking efficient therapeutic approach despite of vaccine. In this study, we have identified a novel cytoplasmic lncRNA, namely rabies virus related lncRNA 1(RVRL1), whose expression in neuronal cells is up-regulated upon the infection of the causative agent of rabies, the neurotropic virus rabies virus (RABV). RVRL1 effectively inhibits RABV infection both in neuronal cells and in a mouse model. RVRL1 binds to EZH2 and disrupts the PRC2 complex, which is consistent with the inverse relationship between RVRL1 expression and the cellular H3K27me3 level. RVRL1 expression positively regulates the expression of PCP4L1 encoding a 10 kD peptide, which is shown to inhibit RABV replication. These findings highlight a novel mechanism for lncRNAs to upregulate the expression of antiviral genes, and define two potential anti-rabies reagents including an antiviral lncRNA and an antiviral peptide.

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LncRNA RVRL1 restricts rabies virus infection by disrupting PRC2 complex [RNA-seq]

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Project description:In-depth genome analyses of viruses from vaccine-derived rabies cases and corresponding live-attenuated oral rabies vaccines

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Rabies-Infected Neurons Can Be Transcriptomically Characterized Despite Changes in Gene Expression

Project description:Cortical circuit tracing using modified rabies virus can identify input neurons making direct monosynaptic connections onto neurons of interest. However, challenges remain in our ability to establish the cell type identity of rabies-labeled input neurons. While transcriptomics may offer an avenue to characterize inputs, the extent of rabies-induced transcriptional changes in distinct neuronal cell types remains unclear and whether these changes preclude characterization of rabies-infected neurons according to established transcriptomic cell types is unknown. We used single-nucleus RNA sequencing to survey the gene expression profiles of rabies-infected neurons and assessed their correspondence with established transcriptomic cell types. We demonstrated that when using transcriptome-wide RNA profiles, rabies-infected cortical neurons can be transcriptomically characterized despite global and cell-type-specific rabies-induced transcriptional changes. Notably, we found differential modulation of neuronal marker gene expression, suggesting that caution should be taken when attempting to characterize rabies-infected cells with single genes or small gene sets.

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Project description:Lyssavirus rabies Genome sequencing

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Project description:Street-strain rabies virus primarily replicates in central nervous system without inducing significant immune response or structural damages on neurons, but the manifested symptoms of rabies indicate inherent neuronal dysfunctions in CNS. To understand the underlying state of rabies virus-infected neurons and find probable mechanisms for the neuronal dysfunction, we performed RNA-Seq at multiple time-points. This dataset provides RNA-Seq results of wild-type and mutant rabies virus-infected neuron transcriptome, with clear differential expressions between conditions. Through comparative analysis of different time-points, we have found that the matrix protein of rabies virus plays an important role in early suppression of host gene expression and maintaining control over immune response and other processes. The signaling pathways previously known to interact with rabies virus were confirmed to be modulated in this dataset, and contribute to neuronal function-associated processes. We have verified the regulation of gene expressions that could impact neuronal functions collectively, and demonstrated in calcium imaging that indeed the oscillation of calcium trace in neurons are influenced by rabies virus infection.

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