Seroprevalence of emerging hepatitis E virus in patients with acute hepatitis between 2004 and 2018 in Csongrád County, Hungary.

OBJECTIVES: Hepatitis E virus (HEV) has recently become endemic in Europe, however, it is often a remnant neglected by clinicians as the causative agent of acute and chronic hepatitis and is often misdiagnosed as a drug-induced liver injury. The infection rate in European pig farms is estimated to be around 15-20%, therefore, the primary source of HEV infections might be poorly prepared pork meat. As HEV infections may occur more often in clinical practice than previously thought, the present paper aims to analyse the seroprevalence of HEV in patients with acute hepatitis over a period of 14 years in Csongrád County, Hungary. METHODS: The sera of 4,270 hepatitis patients collected between 2004-2018 were tested for cumulative anti-HEV IgG/IgM. Furthermore, 170 IgM positive sera were tested for the presence of viral RNA by RT-qPCR. RESULTS: Between 2012-2018, the cumulative seroprevalence has increased 9.18 times, and between 2013-2018, IgM prevalence has increased 12.49 times. Viral RNA was detectable in 12.35% of IgM positive sera. CONCLUSION: The present paper presents data showing that the seroprevalence of hepatitis E virus has increased markedly over the course of the last decade in Hungary and in other European countries as well. The exact reason behind this phenomenon is yet to be determined. To assess the dynamics and the reason for this increase in prevalence, pan-European, multicentre studies should be conducted.

Effect of cortical spreading depression on basal forebrain neurons.

During natural sleep and anesthesia, rhythmic hypo- and hyperpolarizations alternate in cortical pyramidal cells and are reflected as slow (<1 Hz) cortical rhythm at the level of the electroencephalogram (EEG). Membrane potential changes in pyramidal neurons were initially attributed to the rhythmic fluctuation of the cholinergic input as the basal forebrain (BF) neurons fire in synchrony with cortical waves, but a more recent proposal suggested that the slow rhythm was of cortical origin. In the present experiments, interaction between the cortex and the BF was examined in urethane-anesthetized rats. BF neuronal activity was inhibited by local infusion of lidocaine into the substantia innominata in one group of rats, while in another group, the slow cortical rhythm was blocked by inducing spreading depression (SD) in the cortex. Slow cortical rhythm persisted after unilateral lidocaine injection, but rhythmic firing in BF neurons disappeared following SD induction. These findings support the view that slow cortical rhythm is generated in the cortex and transmitted to the BF through descending fibers. According to anatomical data, these fibers can excite cholinergic cells only indirectly as they terminate on non-cholinergic neurons. Thus, timing of activity changes in BF neurons during the slow cortical rhythm might give some clue regarding their transmitter specificity.