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Zika virus infection elicits auto-antibodies to C1q
Zika virus (ZIKV) causes mostly asymptomatic infection or mild febrile illness. However, with an increasing number of patients, various clinical features such as microcephaly, Guillain-Barré syndrome and thrombocytopenia have also been reported. To determine which host factors are related to pathoge...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5789871/ https://www.ncbi.nlm.nih.gov/pubmed/29382894 http://dx.doi.org/10.1038/s41598-018-20185-8 |
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author | Koma, Takaaki Veljkovic, Veljko Anderson, Danielle E. Wang, Lin-Fa Rossi, Shannan L. Shan, Chao Shi, Pei-Yong Beasley, David W. Bukreyeva, Natalya Smith, Jeanon N. Hallam, Steven Huang, Cheng von Messling, Veronika Paessler, Slobodan |
author_facet | Koma, Takaaki Veljkovic, Veljko Anderson, Danielle E. Wang, Lin-Fa Rossi, Shannan L. Shan, Chao Shi, Pei-Yong Beasley, David W. Bukreyeva, Natalya Smith, Jeanon N. Hallam, Steven Huang, Cheng von Messling, Veronika Paessler, Slobodan |
author_sort | Koma, Takaaki |
collection | PubMed |
description | Zika virus (ZIKV) causes mostly asymptomatic infection or mild febrile illness. However, with an increasing number of patients, various clinical features such as microcephaly, Guillain-Barré syndrome and thrombocytopenia have also been reported. To determine which host factors are related to pathogenesis, the E protein of ZIKV was analyzed with the Informational Spectrum Method, which identifies common information encoded by primary structures of the virus and the respective host protein. The data showed that the ZIKV E protein and the complement component C1q cross-spectra are characterized by a single dominant peak at the frequency F = 0.338, suggesting similar biological properties. Indeed, C1q-specific antibodies were detected in sera obtained from mice and monkeys infected with ZIKV. As C1q has been known to be involved not only in immunity, but also in synaptic organization and different autoimmune diseases, a ZIKV-induced anti-C1q antibody response may contribute to the neurological complications. These findings might also be exploited for the design of safe and efficacious vaccines in the future. |
format | Online Article Text |
id | pubmed-5789871 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-57898712018-02-15 Zika virus infection elicits auto-antibodies to C1q Koma, Takaaki Veljkovic, Veljko Anderson, Danielle E. Wang, Lin-Fa Rossi, Shannan L. Shan, Chao Shi, Pei-Yong Beasley, David W. Bukreyeva, Natalya Smith, Jeanon N. Hallam, Steven Huang, Cheng von Messling, Veronika Paessler, Slobodan Sci Rep Article Zika virus (ZIKV) causes mostly asymptomatic infection or mild febrile illness. However, with an increasing number of patients, various clinical features such as microcephaly, Guillain-Barré syndrome and thrombocytopenia have also been reported. To determine which host factors are related to pathogenesis, the E protein of ZIKV was analyzed with the Informational Spectrum Method, which identifies common information encoded by primary structures of the virus and the respective host protein. The data showed that the ZIKV E protein and the complement component C1q cross-spectra are characterized by a single dominant peak at the frequency F = 0.338, suggesting similar biological properties. Indeed, C1q-specific antibodies were detected in sera obtained from mice and monkeys infected with ZIKV. As C1q has been known to be involved not only in immunity, but also in synaptic organization and different autoimmune diseases, a ZIKV-induced anti-C1q antibody response may contribute to the neurological complications. These findings might also be exploited for the design of safe and efficacious vaccines in the future. Nature Publishing Group UK 2018-01-30 /pmc/articles/PMC5789871/ /pubmed/29382894 http://dx.doi.org/10.1038/s41598-018-20185-8 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Koma, Takaaki Veljkovic, Veljko Anderson, Danielle E. Wang, Lin-Fa Rossi, Shannan L. Shan, Chao Shi, Pei-Yong Beasley, David W. Bukreyeva, Natalya Smith, Jeanon N. Hallam, Steven Huang, Cheng von Messling, Veronika Paessler, Slobodan Zika virus infection elicits auto-antibodies to C1q |
title | Zika virus infection elicits auto-antibodies to C1q |
title_full | Zika virus infection elicits auto-antibodies to C1q |
title_fullStr | Zika virus infection elicits auto-antibodies to C1q |
title_full_unstemmed | Zika virus infection elicits auto-antibodies to C1q |
title_short | Zika virus infection elicits auto-antibodies to C1q |
title_sort | zika virus infection elicits auto-antibodies to c1q |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5789871/ https://www.ncbi.nlm.nih.gov/pubmed/29382894 http://dx.doi.org/10.1038/s41598-018-20185-8 |
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