| Item type |
☆紀要論文 / Departmental Bulletin Paper(1) |
| 公開日 |
2017-10-24 |
| タイトル |
|
|
タイトル |
<Review> Neuropathogenesis of Zika Virus Infection: Potential Roles of Antibody-Mediated Pathology |
|
言語 |
en |
| 著者 |
Tsunoda, Ikuo
Omura, Seiichi
Sato, Fumitaka
Kusunoki, Susumu
Fujita, Mitsugu
Park, Ah-Mee
Hasanovic, Faris
Yanagihara, Richard
Nagata, Satoshi
|
| 言語 |
|
|
言語 |
eng |
| キーワード |
|
|
主題 |
Animal Models, Experimental Autoimmune Neuritis, Gangliosides, Placenta, Retrograde Axonal Flow, Theiler’s Murine Encephalomyelitis Virus, Yellow Fever Virus |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
departmental bulletin paper |
| 著者 所属 |
|
|
値 |
Department of Microbiology, Kindai University Faculty of Medicine |
| 著者 所属 |
|
|
値 |
Department of Microbiology, Kindai University Faculty of Medicine |
| 著者 所属 |
|
|
値 |
Department of Microbiology, Kindai University Faculty of Medicine |
| 著者 所属 |
|
|
値 |
Department of Neurology, Kindai University Faculty of Medicine |
| 著者 所属 |
|
|
値 |
Department of Microbiology, Kindai University Faculty of Medicine |
| 著者 所属 |
|
|
値 |
Department of Microbiology, Kindai University Faculty of Medicine |
| 著者 所属 |
|
|
値 |
Department of Pathology, Children’s Hospital Colorado |
| 著者 所属 |
|
|
値 |
Departments of Pediatrics and Tropical Medicine, Medical Microbiology and Pharmacology John A. Burns School of Medicine University of Hawaii |
| 著者 所属 |
|
|
値 |
Center for Drug Design Research, National Institutes of Biomedical Innovation, Health and Nutrition(NIBIOHN) |
| 版 |
|
|
出版タイプ |
NA |
|
出版タイプResource |
http://purl.org/coar/version/c_be7fb7dd8ff6fe43 |
| 出版者 名前 |
|
|
出版者 |
Kindai University Medical Association |
| 書誌情報 |
en : ACTA MEDICA KINDAI UNIVERSITY
巻 41,
号 2,
p. 37-52,
発行日 2016-12
|
| ISSN |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
03866092 |
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
[Abstract] Zika virus(ZIKV) is an enveloped, positive-sense, single-stranded RNA virus that belongs to the genus Flavivirus, family Flaviviridae, which includes many human and animal pathogens, such as dengue virus (DENV),West Nile virus, and Japanese encephalitis virus. In the original as well as subsequent experimental and clinical reports, ZIKV seems to have moderate neurotropism (in animal models) and neurovirulence (in human fetuses), but no neuroinvasiveness (in human adults). Intrauterine ZIKV infection (viral pathology) has been linked to an increased incidence of microcephaly, while increased Guillain- Barre syndrome (GBS) following ZIKV infection is likely immune-mediated (immunopathology). Clinically, in ZIKV infection, antibodies against other flaviviruses, such as DENV, have been detected; these antibodies can cross-react with ZIKV without ZIKV neutralization. In theory, such non-neutralizing antibodies are generated at the expense of decreased production of neutralizing antibodies (“antigenic sin”),leading to poor viral clearance, while the non-neutralizing antibodies can also enhance viral replication in Fc receptor (FcR)-bearing cells via antibody-dependent enhancement (ADE). Here, we propose three potential roles of the antibody-mediated pathogenesis of ZIKV infection: 1) cross-reactive antibodies that recognize ZIKV and neural antigens cause GBS; 2) ZIKV-antibody complex is transported transplacentally via neonatal FcR (FcRn), resulting in fetal infection; and 3) ZIKV-antibody complex is taken up at peripheral nerve endings and transported to neurons in the central nervous system (CNS), by which the virus can enter the CNS without crossing the blood-brain barrier. |
AA0050842X-20161200-0037.pdf (1.3 MB)
