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Viruses
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Neurotropic Viral Pathogens
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Neurotropic Viral Pathogens

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "General Virology".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 12330

Special Issue Editors

Prof. Dr. Thomas E. Lane

E-Mail Website
Guest Editor
Department of Neurobiology and Behavior, University of California, Irvine, CA, USA
Interests: CNS infection
Dr. Orkide Koyuncu

E-Mail Website
Guest Editor
Department of Microbiology and Molecular Genetics, University of California, Irvine, CA, USA
Interests: neuroviral infections
Prof. Dr. Michael J. Buchmeier

E-Mail Website
Guest Editor
Department of Microbiology and Molecular Genetics, University of California, Irvine, CA, USA
Interests: arenavirus; bunyavirales; lassa fever

Special Issue Information

Dear Colleagues,

This Special Issue of Viruses focuses on viral infections of the nervous system (NS) both at the molecular and systems level, including models of viral-induced human neurological disease. The NS is protected against viral infection by several layers of anatomical and physiological barriers. However, most of the human population has been infected with persistent viruses that either establish infection in the NS or can gain access to the NS upon reactivation, causing a wide array of neurological problems ranging from mild symptoms to life-threatening conditions. Moreover, emerging virus infections represent a threat to the NS either by direct transmission to the neural tissue or by triggering inflammation or degeneration of the NS, as we experienced in the Zika virus outbreak and the COVID-19 pandemic. Therefore, it is of great importance to understand the mechanisms underlying viruses’ abilities to access to the NS, establish infection and spread in the neural circuits. Additionally, we need to identify the mechanisms by which these viruses evade immunological attack and how the immune system responds to infection and eliminates these invaders while limiting the severity of immune-mediated neurologic diseases. Greater insight into these questions through discovery-based research will inevitably allow for the development of better therapeutic strategies against latent, chronic or emerging neuroviruses.

Prof. Dr. Thomas E. Lane
Dr. Orkide Ö. Koyuncu
Prof. Dr. Michael J. Buchmeier
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (8 papers)

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Editorial

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3 pages, 156 KiB  
Editorial
An Emerging Conundrum in Nervous System Infections: Balancing Virus Offense and Host Defense
by Lynn Enquist
Viruses 2023, 15(10), 2071; https://doi.org/10.3390/v15102071 - 10 Oct 2023
Viewed by 638
Abstract
Most viral infections begin in the peripheral organs and, as a result, engage the circulatory (blood and lymph) system, releasing more virus particles and other products of the infection (both host and virus gene products) into the circulation [...] Full article
(This article belongs to the Special Issue Neurotropic Viral Pathogens)

Review

Jump to: Editorial

27 pages, 1702 KiB  
Review
The Contribution of Microglia and Brain-Infiltrating Macrophages to the Pathogenesis of Neuroinflammatory and Neurodegenerative Diseases during TMEV Infection of the Central Nervous System
by Ana Beatriz DePaula-Silva
Viruses 2024, 16(1), 119; https://doi.org/10.3390/v16010119 - 13 Jan 2024
Cited by 2 | Viewed by 2366
Abstract
The infection of the central nervous system (CNS) with neurotropic viruses induces neuroinflammation and is associated with the development of neuroinflammatory and neurodegenerative diseases, including multiple sclerosis and epilepsy. The activation of the innate and adaptive immune response, including microglial, macrophages, and T [...] Read more.
The infection of the central nervous system (CNS) with neurotropic viruses induces neuroinflammation and is associated with the development of neuroinflammatory and neurodegenerative diseases, including multiple sclerosis and epilepsy. The activation of the innate and adaptive immune response, including microglial, macrophages, and T and B cells, while required for efficient viral control within the CNS, is also associated with neuropathology. Under healthy conditions, resident microglia play a pivotal role in maintaining CNS homeostasis. However, during pathological events, such as CNS viral infection, microglia become reactive, and immune cells from the periphery infiltrate into the brain, disrupting CNS homeostasis and contributing to disease development. Theiler’s murine encephalomyelitis virus (TMEV), a neurotropic picornavirus, is used in two distinct mouse models: TMEV-induced demyelination disease (TMEV-IDD) and TMEV-induced seizures, representing mouse models of multiple sclerosis and epilepsy, respectively. These murine models have contributed substantially to our understanding of the pathophysiology of MS and seizures/epilepsy following viral infection, serving as critical tools for identifying pharmacological targetable pathways to modulate disease development. This review aims to discuss the host–pathogen interaction during a neurotropic picornavirus infection and to shed light on our current understanding of the multifaceted roles played by microglia and macrophages in the context of these two complexes viral-induced disease. Full article
(This article belongs to the Special Issue Neurotropic Viral Pathogens)
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13 pages, 5732 KiB  
Review
A Pocket Guide to CCR5—Neurotropic Flavivirus Edition
by Amit Garg and Jean K. Lim
Viruses 2024, 16(1), 28; https://doi.org/10.3390/v16010028 - 23 Dec 2023
Viewed by 1015
Abstract
CCR5 is among the most studied chemokine receptors due to its profound significance in human health and disease. The notion that CCR5 is a functionally redundant receptor was challenged through the demonstration of its unique protective role in the context of West Nile [...] Read more.
CCR5 is among the most studied chemokine receptors due to its profound significance in human health and disease. The notion that CCR5 is a functionally redundant receptor was challenged through the demonstration of its unique protective role in the context of West Nile virus in both mice and humans. In the nearly two decades since this initial discovery, numerous studies have investigated the role of CCR5 in the context of other medically important neurotropic flaviviruses, most of which appear to support a broad neuroprotective role for this receptor, although how CCR5 exerts its protective effect has been remarkably varied. In this review, we summarize the mechanisms by which CCR5 controls neurotropic flaviviruses, as well as results from human studies evaluating a genetic link to CCR5, and propose unexplored areas of research that are needed to unveil even more exciting roles for this important receptor. Full article
(This article belongs to the Special Issue Neurotropic Viral Pathogens)
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18 pages, 1148 KiB  
Review
The Impact of Innate Components on Viral Pathogenesis in the Neurotropic Coronavirus Encephalomyelitis Mouse Model
by Brendan T. Boylan, Mihyun Hwang and Cornelia C. Bergmann
Viruses 2023, 15(12), 2400; https://doi.org/10.3390/v15122400 - 09 Dec 2023
Viewed by 1128
Abstract
Recognition of viruses invading the central nervous system (CNS) by pattern recognition receptors (PRRs) is crucial to elicit early innate responses that stem dissemination. These innate responses comprise both type I interferon (IFN-I)-mediated defenses as well as signals recruiting leukocytes to control the [...] Read more.
Recognition of viruses invading the central nervous system (CNS) by pattern recognition receptors (PRRs) is crucial to elicit early innate responses that stem dissemination. These innate responses comprise both type I interferon (IFN-I)-mediated defenses as well as signals recruiting leukocytes to control the infection. Focusing on insights from the neurotropic mouse CoV model, this review discusses how early IFN-I, fibroblast, and myeloid signals can influence protective anti-viral adaptive responses. Emphasis is placed on three main areas: the importance of coordinating the distinct capacities of resident CNS cells to induce and respond to IFN-I, the effects of select IFN-stimulated genes (ISGs) on host immune responses versus viral control, and the contribution of fibroblast activation and myeloid cells in aiding the access of T cells to the parenchyma. By unraveling how the dysregulation of early innate components influences adaptive immunity and viral control, this review illustrates the combined effort of resident CNS cells to achieve viral control. Full article
(This article belongs to the Special Issue Neurotropic Viral Pathogens)
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17 pages, 8929 KiB  
Review
Is the Central Nervous System Reservoir a Hurdle for an HIV Cure?
by Nazanin Mohammadzadeh, Nicolas Chomont, Jerome Estaquier, Eric A. Cohen and Christopher Power
Viruses 2023, 15(12), 2385; https://doi.org/10.3390/v15122385 - 05 Dec 2023
Viewed by 1607
Abstract
There is currently no cure for HIV infection although adherence to effective antiretroviral therapy (ART) suppresses replication of the virus in blood, increases CD4+ T-cell counts, reverses immunodeficiency, and increases life expectancy. Despite these substantial advances, ART is a lifelong treatment for [...] Read more.
There is currently no cure for HIV infection although adherence to effective antiretroviral therapy (ART) suppresses replication of the virus in blood, increases CD4+ T-cell counts, reverses immunodeficiency, and increases life expectancy. Despite these substantial advances, ART is a lifelong treatment for people with HIV (PWH) and upon cessation or interruption, the virus quickly rebounds in plasma and anatomic sites, including the central nervous system (CNS), resulting in disease progression. With recent advances in quantifying viral burden, detection of genetically intact viral genomes, and isolation of replication-competent virus from brain tissues of PWH receiving ART, it has become apparent that the CNS viral reservoir (largely comprised of macrophage type cells) poses a substantial challenge for HIV cure strategies. Other obstacles impacting the curing of HIV include ageing populations, substance use, comorbidities, limited antiretroviral drug efficacy in CNS cells, and ART-associated neurotoxicity. Herein, we review recent findings, including studies of the proviral integration sites, reservoir decay rates, and new treatment/prevention strategies in the context of the CNS, together with highlighting the next steps for investigations of the CNS as a viral reservoir. Full article
(This article belongs to the Special Issue Neurotropic Viral Pathogens)
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26 pages, 859 KiB  
Review
Cell Intrinsic Determinants of Alpha Herpesvirus Latency and Pathogenesis in the Nervous System
by Stephanie Salazar, Khanh T. Y. Luong and Orkide O. Koyuncu
Viruses 2023, 15(12), 2284; https://doi.org/10.3390/v15122284 - 22 Nov 2023
Viewed by 1555
Abstract
Alpha herpesvirus infections (α-HVs) are widespread, affecting more than 70% of the adult human population. Typically, the infections start in the mucosal epithelia, from which the viral particles invade the axons of the peripheral nervous system. In the nuclei of the peripheral ganglia, [...] Read more.
Alpha herpesvirus infections (α-HVs) are widespread, affecting more than 70% of the adult human population. Typically, the infections start in the mucosal epithelia, from which the viral particles invade the axons of the peripheral nervous system. In the nuclei of the peripheral ganglia, α-HVs establish a lifelong latency and eventually undergo multiple reactivation cycles. Upon reactivation, viral progeny can move into the nerves, back out toward the periphery where they entered the organism, or they can move toward the central nervous system (CNS). This latency–reactivation cycle is remarkably well controlled by the intricate actions of the intrinsic and innate immune responses of the host, and finely counteracted by the viral proteins in an effort to co-exist in the population. If this yin-yang- or Nash-equilibrium-like balance state is broken due to immune suppression or genetic mutations in the host response factors particularly in the CNS, or the presence of other pathogenic stimuli, α-HV reactivations might lead to life-threatening pathologies. In this review, we will summarize the molecular virus–host interactions starting from mucosal epithelia infections leading to the establishment of latency in the PNS and to possible CNS invasion by α-HVs, highlighting the pathologies associated with uncontrolled virus replication in the NS. Full article
(This article belongs to the Special Issue Neurotropic Viral Pathogens)
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19 pages, 1708 KiB  
Review
Molecular and Cellular Mechanisms Underlying Neurologic Manifestations of Mosquito-Borne Flavivirus Infections
by Britanie M. Blackhurst and Kristen E. Funk
Viruses 2023, 15(11), 2200; https://doi.org/10.3390/v15112200 - 31 Oct 2023
Viewed by 1416
Abstract
Flaviviruses are a family of enveloped viruses with a positive-sense RNA genome, transmitted by arthropod vectors. These viruses are known for their broad cellular tropism leading to infection of multiple body systems, which can include the central nervous system. Neurologic effects of flavivirus [...] Read more.
Flaviviruses are a family of enveloped viruses with a positive-sense RNA genome, transmitted by arthropod vectors. These viruses are known for their broad cellular tropism leading to infection of multiple body systems, which can include the central nervous system. Neurologic effects of flavivirus infection can arise during both acute and post-acute infectious periods; however, the molecular and cellular mechanisms underlying post-acute sequelae are not fully understood. Here, we review recent studies that have examined molecular and cellular mechanisms that may contribute to neurologic sequelae following infection with the West Nile virus, Japanese encephalitis virus, Zika virus, dengue virus, and St. Louis encephalitis virus. Neuronal death, either from direct infection or due to the resultant inflammatory response, is a common mechanism by which flavivirus infection can lead to neurologic impairment. Other types of cellular damage, such as oxidative stress and DNA damage, appear to be more specific to certain viruses. This article aims to highlight mechanisms of cellular damage that are common across several flavivirus members and mechanisms that are more unique to specific members. Our goal is to inspire further research to improve understanding of this area in the hope of identifying treatment options for flavivirus-associated neurologic changes. Full article
(This article belongs to the Special Issue Neurotropic Viral Pathogens)
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31 pages, 1731 KiB  
Review
Polyomavirus Wakes Up and Chooses Neurovirulence
by Arrienne B. Butic, Samantha A. Spencer, Shareef K. Shaheen and Aron E. Lukacher
Viruses 2023, 15(10), 2112; https://doi.org/10.3390/v15102112 - 18 Oct 2023
Viewed by 2113
Abstract
JC polyomavirus (JCPyV) is a human-specific polyomavirus that establishes a silent lifelong infection in multiple peripheral organs, predominantly those of the urinary tract, of immunocompetent individuals. In immunocompromised settings, however, JCPyV can infiltrate the central nervous system (CNS), where it causes several encephalopathies [...] Read more.
JC polyomavirus (JCPyV) is a human-specific polyomavirus that establishes a silent lifelong infection in multiple peripheral organs, predominantly those of the urinary tract, of immunocompetent individuals. In immunocompromised settings, however, JCPyV can infiltrate the central nervous system (CNS), where it causes several encephalopathies of high morbidity and mortality. JCPyV-induced progressive multifocal leukoencephalopathy (PML), a devastating demyelinating brain disease, was an AIDS-defining illness before antiretroviral therapy that has “reemerged” as a complication of immunomodulating and chemotherapeutic agents. No effective anti-polyomavirus therapeutics are currently available. How depressed immune status sets the stage for JCPyV resurgence in the urinary tract, how the virus evades pre-existing antiviral antibodies to become viremic, and where/how it enters the CNS are incompletely understood. Addressing these questions requires a tractable animal model of JCPyV CNS infection. Although no animal model can replicate all aspects of any human disease, mouse polyomavirus (MuPyV) in mice and JCPyV in humans share key features of peripheral and CNS infection and antiviral immunity. In this review, we discuss the evidence suggesting how JCPyV migrates from the periphery to the CNS, innate and adaptive immune responses to polyomavirus infection, and how the MuPyV-mouse model provides insights into the pathogenesis of JCPyV CNS disease. Full article
(This article belongs to the Special Issue Neurotropic Viral Pathogens)
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