Abstract
Borna disease virus (BDV) is a neurotropic, enveloped, non-segmented, negative-stranded RNA virus that infects a wide variety of vertebrate species from birds to humans across a broad global geographic distribution. Animal symptomatology range from asymptomatic infection to behavioral abnormalities to acute meningoencephalitis. Asymptomatic BDV infection has been shown to be more frequent than conventionally estimated. However, the molecular mechanism(s) underyling asymptomatic BDV infection remain largely unknown. Here, based on real-time quantitative PCR and Western blotting, a total of 18 horse hippocampi were divided into BDV-infected (n = 8) and non-infected control (n = 10) groups. A gas chromatography coupled with mass spectrometry (GC-MS) metabolomic approach, in conjunction with multivariate statistical analysis, was used to characterize the hippocampal metabolic changes associated with asymptomatic BDV infection. Multivariate statistical analysis showed a significant discrimination between the BDV-infected and control groups. BDV-infected hippocampi were characterized by lower levels of D-myo-inositol-1-phosphate, glutamate, phosphoethanolamine, heptadecanoic acid, and linoleic acid in combination with a higher level of ammonia. These differential metabolites are primarily involved in glutamate and lipid metabolism. These finding provide an improved understanding of hippocampal changes associated with asymptomatic BDV infection.
Highlights
Borna disease virus (BDV), the causative agent of Borna disease (BD) that owes its name to the German town of Borna, Saxony where a large number of horses died of a fatal neurologic disease during an 1885 epidemic [1], is a neurotropic, non-cytolytic, enveloped, non-segmented, negative-stranded RNA virus with a genome size of approximately 8.9 kb and replicates and transcribes itself in the nuclei of infected cells [2]
Identification of BDV Infection in Hippocampal Tissue For Realtime quantitative PCR (RT-qPCR) assays, negative control samples in each assay were consistently negative, and Cq values of positive control samples were less than 25 cycles
These findings indicate that the RT-qPCR system functioned normally
Summary
Borna disease virus (BDV), the causative agent of Borna disease (BD) that owes its name to the German town of Borna, Saxony where a large number of horses died of a fatal neurologic disease during an 1885 epidemic [1], is a neurotropic, non-cytolytic, enveloped, non-segmented, negative-stranded RNA virus with a genome size of approximately 8.9 kb and replicates and transcribes itself in the nuclei of infected cells [2]. Classical BD has traditionally occurred in geographically restricted areas in Germany, Austria, Switzerland, and Lichtenstein [3,4,5], signs of BDV infection have been reported in horses and several other mammalian species across a broader range of countries, including Israel, Iran, Japan, Australia, the U.S, and several other European countries [6], suggesting that BDV is more widespread than conventionally believed. BDV infection in horses can result in peracute, acute, or subacute BD with meningoencephalitis. Since BDV-specific antibodies or RNAs have been found in clinically healthy horses in many geographic areas including China [20,21,22,23,24], asymptomatic infection appears to be more frequent than conventionally estimated. The underlying mechanism(s) of asymptomatic BDV infection in the horse central nervous system (CNS) have not been adequately characterized
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