Вирус Zika усугубляет энцефаломиэлит, вызывая производство хемокина Т в астроцитах.
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Kamiyama Naganori, Saechue Benjawan, Sachi Nozomi, Chalalai Thanyakorn, Dewayani Astri, Okamoto Masaaki, Ozaka Sotaro, Soga Yasuhiro, Kagoshima Yomei, Ekronarongchai Supanuch, Hidano Shinya, Tsuda Makoto, Kobayashi Takashi
Аннотация
Оригинал публикации
Zika virus exacerbates encephalomyelitis by inducing the production of T cell-attracting chemokines in astrocytes.
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.