Table_1.XLS
Penelope Koraka
Byron E. E. Martina
Henk-Jan van den Ham
Fatiha Zaaraoui-Boutahar
Wilfred van IJcken
Jouke Roose
Geert van Amerongen
Arno Andeweg
Albertus D. M. E. Osterhaus
10.3389/fmicb.2018.00397.s002
https://frontiersin.figshare.com/articles/dataset/Table_1_XLS/6004175
<p>Rabies is an important neglected disease, characterized by invariably fatal encephalitis. Several studies focus on understanding the pathogenic mechanisms of the prototype lyssavirus rabies virus (RABV) infection, and little is known about the pathogenesis of rabies caused by other lyssaviruses. We sought to characterize the host response to Duvenhage virus infection and compare it with responses observed during RABV infection by gene expression profiling of brains of mice with the respective infections. We found in both infections differentially expressed genes leading to increased expression of type I interferons (IFNs), chemokines, and proinflammatory cytokines. In addition several genes of the IFN signaling pathway are up-regulated, indicating a strong antiviral response and activation of the negative feedback mechanism to limit type I IFN responses. Furthermore we provide evidence that in the absence of significant neuronal apoptotic death, cell death of neurons is mediated via the pyroptotic pathway in both infections. Taken together, we have identified several genes and/or pathways for both infections that could be used to explore novel approaches for intervention strategies against rabies.</p>
2018-03-20 08:20:49
rabies
Duvenhage virus
genomics
pyroptosis
innate immune response
caspase-1