Abstract
INTRODUCTION: In severe cases, an infection with the Borna Disease Virus 1 (BoDV-1), the causative agent of Borna disease in horses, sheep, and other domestic mammals, was reported to be accompanied by cognitive dysfunctions, seizures, deep coma, or severe to fatal encephalitis in humans. In addition, asymptomatic or mild courses of BoDV-1 infection are discussed to act as a co-factor in the etiology of Major Depressive Disorder (MDD). Previously, studies using electroencephalography (EEG) reported BoDV-1-dependent changes in event-related potentials (ERPs), thus indicating the use and added value of non-invasive studies in Borna research. METHODS: Here, we examined possible connections between BoDV-1 status, EEG restingstate alpha activity, and serum levels of pro-inflammatory Interleukin 6 (IL-6) and Interleukin 8 (IL-8) in MDD patients and in a comparison group of adults without MDD diagnosis. RESULTS: Interestingly, for both groups, we revealed a comparable high number of BoDV-1 positive and BoDV-1 negative participants. Compared to adults without MDD diagnosis, MDD patients showed a decrease in their relative EEG alpha power at posterio-central, but increased values at anterio-central electrode sites. Most important, no group-dependent effect of BoDV-1 status on EEG resting-state activity had been observed. Compared to BoDV-1 positive and negative adults without MDD diagnosis, as well as BoDV-1 positive MDD patients, BoDV-1 negative MDD patients revealed a comparatively weak significant negative correlation between relative fronto-central EEG alpha power and concentrations of pro-inflammatory IL-8. DISCUSSION: Taken together, our data confirm MDD-dependent alterations in EEG resting-state alpha activity, which, however, were not accompanied by major BoDV-1 dependent neurophysiological or immunological effects. Future - probably more invasive - studies further have to clarify the significance of the observed negative correlation between relative fronto-central EEG alpha power and concentrations of pro-inflammatory IL-8.