ArticleInternational immunology2026
Zika virus exacerbates encephalomyelitis by inducing the production of T cell-attracting chemokines in astrocytes.
Article in International immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Recent outbreaks of the ZIKA virus (ZIKV) in Brazil and Puerto Rico have been linked to an increase in the incidence of fetal microcephaly and Guillain-Barré syndrome. In addition, although a causal relationship remains unproven, ZIKV has been found in the brains of multiple sclerosis (MS) patients, prompting interest in a possible link. The present study aimed to elucidate the role of ZIKV in the pathogenesis of MS. ZIKV-infected mice with experimental autoimmune encephalomyelitis (EAE) exhibited aggravated EAE symptoms with significant demyelination of the central nervous system (CNS). Moreover, ZIKV infection promoted pathogenic T cell infiltration into the CNS by enhancing the expression of chemokines for C-C motif chemokine receptor 2 (CCR2) in astrocytes, which was dependent on tumor necrosis factor receptor-associated factor 6 (TRAF6) signaling. Propagermanium, a CCR2 inhibitor, prevented ZIKV-induced exacerbation of EAE in mice. These findings highlight the critical role of TRAF6 signaling in the progression of neurological disorders caused by ZIKV infection.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.