%0 Journal Article
%A Grut, Viktor
%A Biström, Martin
%A Salzer, Jonatan
%A Stridh, Pernilla
%A Jons, Daniel
%A Gustafsson, Rasmus
%A Fogdell-Hahn, Anna
%A Huang, Jesse
%A Butt, Julia Anna
%A Lindam, Anna
%A Alonso-Magdalena, Lucia
%A Bergström, Tomas
%A Kockum, Ingrid
%A Waterboer, Tim
%A Olsson, Tomas
%A Zetterberg, Henrik
%A Blennow, Kaj
%A Andersen, Oluf
%A Nilsson, Staffan
%A Sundström, Peter
%T Human herpesvirus 6A and axonal injury before the clinical onset of multiple sclerosis.
%J Brain
%V 147
%N 1
%@ 0006-8950
%C Oxford
%I Oxford Univ. Press
%M DKFZ-2023-02294
%P 177-185
%D 2024
%Z 2024 Jan 4;147(1):177-185
%X Recent research indicates that multiple sclerosis is preceded by a prodromal phase with elevated levels of serum neurofilament light chain (sNfL), a marker of axonal injury. The effect of environmental risk factors on the extent of axonal injury during this prodrome is unknown. Human herpesvirus 6A (HHV-6A) is associated with an increased risk of developing multiple sclerosis. The objective of this study was to determine if HHV-6A serostatus is associated with the level of sNfL in the multiple sclerosis prodrome, which would support a causative role of HHV-6A. A nested case-control study was performed by crosslinking multiple sclerosis registries with Swedish biobanks. Individuals with biobank samples collected before the clinical onset of multiple sclerosis were included as cases. Controls without multiple sclerosis were randomly selected, matched for biobank, sex, sampling date and age. Serostatus of HHV-6A and Epstein-Barr virus (EBV) was analysed with a bead-based multiplex assay. The concentration of sNfL was analysed with Single molecule array technology. The association between HHV-6A serology and sNfL was assessed by stratified t-tests and linear regressions, adjusted for EBV serostatus and sampling age. Within-pair ratios of HHV-6A seroreactivity and sNfL were calculated for each case and its matched control. To assess the temporal relationship between HHV-6A antibodies and sNfL, these ratios were plotted against the time to the clinical onset of multiple sclerosis and compared using locally estimated scatterplot smoothing regressions with 95
%K Epstein-Barr virus (Other)
%K axonal injury (Other)
%K human herpesvirus 6-A (Other)
%K multiple sclerosis (Other)
%K neurofilament light chain (Other)
%F PUB:(DE-HGF)16
%9 Journal Article
%$ pmid:37930324
%R 10.1093/brain/awad374
%U https://inrepo02.dkfz.de/record/285259