Difference in pathogenesis between herpes simplex virus type 1 encephalitis and tick-borne encephalitis demonstrated by means of cerebrospinal fluid markers of glial and neuronal destruction

Abstract

We determined the extent of neuronal and glial cell destruction in 13 patients with herpes simplex type 1 (HSV-1) encephalitis, 15 patients with tick-borne encephalitis (TBE), and 20 noninfectious controls by analyzing the cerebrospinal fluid (CSF) concentrations of neurofilament protein (a marker of neurons, mainly axons), neuron-specific enolase (a marker of neurons, mainly somas), glial fibrillary acidic protein, and S-100 protein (markers of astrocytes). In addition, in patients with HSV-1 encephalitis CSF samples were collected serially before 7, 8-14, and 18-49 days and 3-10 months after the onset of neurological symptoms. In the acute stage of HSV-1 encephalitis we found markedly higher CSF levels of the cell damage markers than in patients with TBE. The concentration of cell damage markers in HSV-1 encephalitis decreased within 45 days after acute infection, except for neurofilament protein. The CSF concentrations of neurofilament protein increased during the second week, remained extremely high throughout the next month, and decrease thereafter. The changes in these markers of neuronal and glial destruction demonstrate the neuronal and astroglial cell damage during the first month after HSV-1 encephalitis. In contrast, most patients with TBE had signs only of slight astrogliosis, except for two patients with paresis.

A human peripheral blood monocyte-derived subset acts as pluripotent stem cells

“…4B). These mature cells were further characterized by immunostaining for NSE, NF, and MAP-1B, which are common neuronal markers (28,29). After 3 d of treatment, 25% of the cells displayed a robust immunostaining for these three proteins, and after 5-8 d this staining was detected in Ϸ90% of the cells and was also observed in their processes, especially with regards to MAP-1B (Fig.…”

Neurofilaments and tau proteins in cerebrospinal fluid and serum in dementias and neuroinflammation

“…Alterations in neurofilaments have been observed in multiple neurological diseases including AD (ref. 5,[38][39][40][41][42][43] ). Specific subclasses of neurons varying in the NF content in different regions of the central nervous system have been described 44 .…”

Biomarkers of Encephalitis

“…The concentrations and kinetics of these markers in HSE imply that they may be used as brain damage markers to follow individual patients longitudinally or to evaluate therapeutics. Studahl et al followed neuronal and astroglial marker proteins for up to 6 months in patients with HSE and found markedly higher CSF levels of neuron specific enolase (NSE), neurofilament protein, GFAP and S100 in the acute stage of HSE that was decreased within 45 days after acute infection (Studahl et al 2000). Although high levels of these markers were associated with neurological damage in other acute CNS damaging disorders, such as cerebral infarction (S100 and GFAP) (Aurell et al 1991), neonatal asphyxia (Blennow et al 1995), and after cardiac arrest (NSE) (Karkela et al 1993) Studahl et al were not able to evaluate the prognostic use of these CSF markers in HSE.…”

“…duration of disease before start of treatment, age, localization of the infected area and size of hemorrhagic necrosis) can influence the clinical outcome. Bigger cohorts may be needed to determine whether concentrations are correlated with clinical outcome (Studahl et al 2000). Additional biomarker that might indicate the severity and progression of cerebral injury in HSE is soluble Fas (sFas) which is involved in apoptosis through the Fas/Fas Ligand pathway (Sabri et al 2006).…”