Neurological Diseases Caused by Flavivirus Infections

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: closed (15 October 2023) | Viewed by 4719

Special Issue Editors


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Guest Editor
School of Public Health, Sun Yat-sen University, Guangzhou 510080, China
Interests: flavivirus; immunology; virology; antiviral drugs; vaccines
Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China
Interests: flavivirus; virus-host interaction; immune evasion; antiviral drugs

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Guest Editor
Department of Neurology, Raigmore Hospital, NHS Highlands, Inverness IV2 3UJ, UK
Interests: neurology; neuroepidemiology; tropical neurology; inflammatory neurological disorders

Special Issue Information

Flaviviruses are enveloped, single positive-stranded RNA viruses belonging to the Flaviviridae family and transmitted by arthropods such as mosquitoes and ticks. The genus includes vector-borne neurotropic viruses such as the Japanese encephalitis virus (JEV), Zika virus (ZIKV), Dengue virus (DENV), West Nile virus (WNV), tick-borne encephalitis virus (TBEV), etc. Infections from these viruses can cause neurological diseases affecting the nervous system and brain. For example, several viruses including JEV, WNV and TBEV in this genus can cause viral encephalitis. Moreover, ZIKV infection during pregnancy can cause infants to be born with microcephaly and other congenital malformations, known as congenital Zika syndrome. Infection with ZIKV in adults and children is also associated with other neurologic complications, including Guillain-Barré syndrome, neuropathy and myelitis. Currently, no vaccine is yet available for the prevention or treatment of infections from these viruses. There is an urgent need for further exploration and in-depth research into these neurotropic viruses.

This Special Issue will cover the recent developments in all flaviviruses’ biology, including epidemiology, pathogenesis, vaccines, animal models, treatment strategies and clinical management of the disease. We welcome the submission of research articles, review articles, and short communications related to this Special Issue.

Dr. Zhenjian He
Dr. Xun Zhu
Dr. Francisco Javier Javier Carod-Artal
Guest Editors

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Keywords

  • flavivirus
  • neurological diseases
  • neuroinflammation
  • virus–host interaction
  • immune evasion
  • epidemiology
  • antiviral drugs
  • vaccines

Published Papers (3 papers)

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Research

12 pages, 1337 KiB  
Article
Results of Tick-Borne Encephalitis Virus (TBEV) Diagnostics in an Endemic Area in Southern Germany, 2007 to 2022
by Philipp Steininger, Armin Ensser, Antje Knöll and Klaus Korn
Viruses 2023, 15(12), 2357; https://doi.org/10.3390/v15122357 - 30 Nov 2023
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Abstract
Tick-borne encephalitis virus (TBEV) is the most important tick-transmitted neurotropic flavivirus in Europe and Asia. Our analysis aimed to investigate the contribution of TBEV-specific antibody detection by serological assays and TBEV RNA detection by real-time PCR to the diagnosis of tick-borne encephalitis (TBE). [...] Read more.
Tick-borne encephalitis virus (TBEV) is the most important tick-transmitted neurotropic flavivirus in Europe and Asia. Our analysis aimed to investigate the contribution of TBEV-specific antibody detection by serological assays and TBEV RNA detection by real-time PCR to the diagnosis of tick-borne encephalitis (TBE). We analyzed data from 3713 patients from 16 years of laboratory TBEV diagnostics in an endemic area in Southern Germany. During this period, 126 cases of TBE were diagnosed. TBEV-specific IgM ELISA tests showed a high clinical sensitivity (96.8%) and a very high clinical specificity (99.7%). In immunocompetent patients, TBE was reliably diagnosed by detection of TBEV IgM antibodies in serum. Intrathecal TBEV IgG antibody synthesis was detected in 46 of 84 (55%) cases by analysis of paired serum and cerebrospinal fluid (CSF) samples. None of the 87 immunocompetent TBE patients tested had detectable TBEV RNA in serum or CSF. In contrast, in two TBE patients without TBEV-specific antibodies, diagnosis could only be made by the detection of TBEV RNA in CSF. Both patients had previously been treated with the B cell-depleting antibody rituximab. Therefore, in patients with CNS infection and humoral immunodeficiency, it is necessary to include TBEV PCR in the diagnostic approach. Full article
(This article belongs to the Special Issue Neurological Diseases Caused by Flavivirus Infections)
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28 pages, 9970 KiB  
Article
Morphological and Molecular Changes in the Cortex and Cerebellum of Immunocompetent Mice Infected with Zika Virus
by Aura Caterine Rengifo, Jorge Rivera, Diego Alejandro Álvarez-Díaz, Julián Naizaque, Gerardo Santamaria, Sheryll Corchuelo, Claudia Yadira Gómez and Orlando Torres-Fernández
Viruses 2023, 15(8), 1632; https://doi.org/10.3390/v15081632 - 27 Jul 2023
Cited by 3 | Viewed by 1579
Abstract
Zika virus (ZIKV) disease continues to be a threat to public health, and it is estimated that millions of people have been infected and that there have been more cases of serious complications than those already reported. Despite many studies on the pathogenesis [...] Read more.
Zika virus (ZIKV) disease continues to be a threat to public health, and it is estimated that millions of people have been infected and that there have been more cases of serious complications than those already reported. Despite many studies on the pathogenesis of ZIKV, several of the genes involved in the malformations associated with viral infection are still unknown. In this work, the morphological and molecular changes in the cortex and cerebellum of mice infected with ZIKV were evaluated. Neonatal BALB/c mice were inoculated with ZIKV intraperitoneally, and the respective controls were inoculated with a solution devoid of the virus. At day 10 postinoculation, the mice were euthanized to measure the expression of the markers involved in cortical and cerebellar neurodevelopment. The infected mice presented morphological changes accompanied by calcifications, as well as a decrease in most of the markers evaluated in the cortex and cerebellum. The modifications found could be predictive of astrocytosis, dendritic pathology, alterations in the regulation systems of neuronal excitation and inhibition, and premature maturation, conditions previously described in other models of ZIKV infection and microcephaly. Full article
(This article belongs to the Special Issue Neurological Diseases Caused by Flavivirus Infections)
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11 pages, 1142 KiB  
Article
New Neutralizing Epitope Exposed on the Domain II of Tick-Borne Encephalitis Virus Envelope Glycoprotein E
by Andrey Matveev, Yana Khlusevich, Irina Kozlova, Leonid Matveev, Lyudmila Emelyanova, Artem Tikunov, Ivan Baykov and Nina Tikunova
Viruses 2023, 15(6), 1256; https://doi.org/10.3390/v15061256 - 26 May 2023
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Abstract
Orthoflavivirus encephalitidis, formerly tick-borne encephalitis virus (TBEV), belongs to the Orthoflavivirus genus. TBEV is transmitted by tick bites and infection with TBEV can lead to serious disorders of the central nervous system. In this study, a new protective monoclonal mouse antibody (mAb) [...] Read more.
Orthoflavivirus encephalitidis, formerly tick-borne encephalitis virus (TBEV), belongs to the Orthoflavivirus genus. TBEV is transmitted by tick bites and infection with TBEV can lead to serious disorders of the central nervous system. In this study, a new protective monoclonal mouse antibody (mAb) FVN-32, with high binding activity to glycoprotein E of TBEV, was selected and examined in post exposure prophylaxis in a mouse model of TBEV infection. BALB/c mice were injected mAb FVN-32 at doses of 200 μg, 50 μg, and 12.5 μg per mouse one day after a TBEV challenge. mAb FVN-32 showed 37.5% protective efficacy when administered at doses of 200 μg and 50 μg per mouse. The epitope for protective mAb FVN-32 was localized in TBEV glycoprotein E domain I+II, using a set of truncated fragments of glycoprotein E. Additionally, the target site recognized by mAb FVN-32 was defined using combinatorial libraries of peptides. Three-dimensional modeling revealed that the site is dspatially close to the fusion loop, but does not come into contact with it, and is localized in a region between 247 and 254 amino acid residues on the envelope protein. This region is conserved among TBEV-like orthoflaviviruses. Full article
(This article belongs to the Special Issue Neurological Diseases Caused by Flavivirus Infections)
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