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Increased level of compleasomes in cerebrospinal fluid of patients with herpes simplex encephalitis

Journal article
Authors Ewa Johansson
Stefan Lange
Tomas Bergström
Merna Oshalim
Ivar Lönnroth
Marie Studahl
Published in Journal of Neurovirology
Volume 24
Issue 6
Pages 702-711
ISSN 1355-0284
Publication year 2018
Published at Institute of Biomedicine, Department of Infectious Medicine
Pages 702-711
Language en
Keywords Herpes simplex encephalitis, Cerebrospinal fluid, Compleasome, Antisecretory factor, Proteasome, central-nervous-system, von-willebrand-factor, antisecretory factor, peptide af-16, virus encephalitis, complement, activation, pcr, hsv
Subject categories Neurosciences, Virology


Herpes simplex encephalitis (HSE) is a common cause of viral encephalitis (HSV-1) characterised by pronounced inflammation and elevated intracranial pressure. We have shown in a rat model that HSV-1 infection causes an interaction between complement factors and proteasomes, leading to formation of proteasome/complement complexes (compleasomes). Exposure of the proteasome regulatory subunit antisecretory factor 1 (AF1) leads to a decrease in intracranial pressure. The aim of this study was to evaluate the acute and prolonged formation of compleasomes in cerebrospinal fluid (CSF) from patients with HSE. Cerebrospinal fluid samples (n=55) from 24 HSE patients were analysed for compleasome complexes. Samples from healthy controls (n=23) and patient controls (n=27) served as baseline information. Sandwich enzyme-linked immunosorbent assay (ELISA) for proteasomes and their complex formation with complement factor 3 or 4, and Western blot for C3 activation were performed on CSF samples. Increased compleasome formation, both presenting as an initial formation and showing exposure of subunit AF1 in the compleasomes, was found in CSF samples drawn from patients with HSE compared with samples from the control groups (p<0.0005). The total protein CSF concentration was equal in all groups. The levels were higher in the acute phase compared with late in the disease course (p<0.0005). Complement 3 breakdown product iC3b was detected in CSF samples of the HSE patients. The early increased formation of compleasomes in CSF suggests that this complex may be involved in host defence against HSE.

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