














































The Role of the Gut Microbiome in Neuromodulation Therapies as a Potential Treatment Adjunct for Multiple Sclerosis


Berkeley
Pharma Tech
Journal of Medicine

Correspondence: 
ftobomanu@uchicago.edu

Keywords:
Neuroinvasive infections 
SARS-CoV-2
Central Nervous System (CNS)
Neurological complications
Viral pathogenesis

Submitted December 13, 2023 
Accepted August 19, 2024
Published December 27, 2024

Full Open Access

Creative Commons Attribution 
License 4.0

Abstract
Infectious diseases have had significant threats to human health, with neurological 
complications as a challenging frontier in the realm of medical science. Neuroinvasive 
infections are caused by viruses, bacteria, fungi, or protozoa and can lead to various 
neurological problems such as meningitis, encephalitis, abscesses, myelitis, and 
neuromuscular dysfunction. Among these pathogens, viruses, including Dengue, West 
Nile, and most recently SARS-CoV-2, have emerged as potent human pathogens capable 
of inflicting severe damage to the central nervous system (CNS), culminating in 
hemorrhagic diseases.

Exploring the Intricacies of Neuroinvasive 
Infections: A Comprehensive Analysis of 
SARS-CoV-2’s Impact on the Nervous 
System
By: Fantasia Obomanu, Emily Woo, Sunanya Adoni, Verdasri Surada



1. Introduction

1.1 The Multifaceted World of Neuroinvasive Infections

The pathogenesis of neuroinvasive infections is characterized by the
remarkable ability of these pathogens to infiltrate the nervous system. They
exploit a mechanism known as axonal transport, which utilizes the physical
structures of axons– the elongated projections of nerve cells—to move
within the host (infected person). By doing so, they evade immune
responses focused on targeting them in other parts of the body. The
inflammatory responses triggered by these infections resemble those
observed autoimmune disorders, involving microglial proliferation
(responses of immune cells in the brain), blood-brain barrier dysfunction (a
protective barrier in the brain), and immune cell infiltration.

The intricate interplay between pathogens, the nervous system, and the
resulting neurological consequences forms the core of our exploration.The
intricacy lies in the multifaceted ways these pathogens can engage with the
nervous system, potentially leading to a spectrum of neurological
consequences. This dynamic relationship is not a unidirectional process;
rather, it involves a reciprocal influence where the pathogen can impact the
nervous system, and vice versa. Understanding this intricate interplay is
crucial for researchers delving into the mechanisms of neuroinvasion and
subsequent neurological manifestations.

The COVID-19 pandemic serves as a great example, illustrating the practical
implications of the complex relationship between pathogens and the
nervous system. SARS-CoV-2, the virus responsible for COVID-19, has not
only demonstrated the ability to infect respiratory cells but has also revealed
a neurotropic potential. The virus can enter the central nervous system,
leading to a range of neurological complications, from mild symptoms like
loss of smell to more severe conditions such as encephalitis. This
manifestation underscores the intricate nature of the interplay between
pathogens and the nervous system. The unprecedented scale and global
impact of the COVID-19 pandemic further emphasize the urgency of

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comprehending these complex interactions for effective medical research
and intervention.

In tandem with these neuroinvasive infections, the COVID-19 pandemic
has presented a global health crisis of unprecedented proportions. The novel
coronavirus, SARS-CoV-2, has unveiled the complex landscape of
neurological complications, thrusting the nervous system into the forefront
of medical research.

Figure 1. Model of External Transport and Neuron-Neuron or Neuron
Non-Neuron Cells Propagation. (A) Murine primary mixed neuron cultures (PMNC)
grown in Xonachip microfluidic compartmentalized chambers. These devices allow fluidic
isolation of axons. (B) Electron microscopy images of infected PMNC (C) Model of
HCoV OC-43 propagation

1.2 Purpose of the Review

The purpose of this review is to investigate the potential therapeutic
interventions aimed at mitigating the neurological damage inflicted by the
SARS-CoV-2 pathogen, with a particular focus on the prevention of
neurological consequences resulting from an infected host. The evolving
landscape of neuroinvasive infections and the continuous battle against the
repercussions of SARS-CoV-2 on the nervous system beckon us to chart a
course toward effective therapeutic strategies that can offer relief and hope
to those suffering from the consequences of COVID-19.

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2. Significance of the Global Impact & Damage of
SARS-CoV-2

The global impact of SARS-CoV-2 has been staggering, with approximately
600 million people affected by COVID-19 as of 2022.1 SARS-CoV-2, akin
to neuroinvasive infections, can cause a wide array of neurological problems.
These problems include anosmia, ageusia, headaches, confusion, delirium,
strokes, encephalitis, Guillain-Barre syndrome, and ischemic stroke.2 This
disease affects multiple organs and systems in the body, leading to severe and
long-term complications.3

The mechanism through which SARS-CoV-2 gains access to the central
nervous system (CNS) is a subject of ongoing investigation. It is suggested
that the virus may exploit multiple routes, including crossing the protective
blood-brain barrier (BBB) or interacting with the ACE2 receptor, which is
expressed in the brain. The direct assault of SARS-CoV-2 on the CNS,
coupled with the abnormal immune response within the CNS, contributes
to the complex nature of the disease.

Beyond its respiratory manifestations, COVID-19 has revealed its capacity
to inflict neurological deficits at different stages of the infection.
Neurological deficits associated with COVID-19 include headache, changes
in sense of smell and taste, muscle pain, mood disturbance (depression,
anxiety), weakness of the limbs, loss of consciousness, seizure, confusion,
vision changes, acute encephalopathy, cerebrovascular events, acute
inflammatory syndromes, and seizures. These deficits can occur in both
adults and preterm infants with low birth weight born to COVID-19
affected mothers. Neurological sequelae after critical COVID-19 disease
can result in substantial deficits in activities of daily living and reduced
health-related quality of life. Moreover, it can leave a lasting imprint on the
nervous system, causing post-infectious complications and long-term effects
that are yet to be fully understood.

The emergence of SARS-CoV-2 variants, characterized by their high
mutation rates, has posed further challenges to global health. The diversity

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in the presentation of COVID-19 symptoms, coupled with the complexities
of diagnosing the disease, has added layers of difficulty to its management.4

3. Neurological Damage Caused by SARS-CoV-2

The evidence of neurological damage caused by SARS-CoV-2 is becoming
increasingly clear, as various studies have uncovered potential mechanisms
underlying this damage. Autopsy analyses of COVID-19 patients, observed
using electron microscopy and fluorescence microscopy, have shown the
presence of SARS-CoV-2 proteins in vital organs, including the brain,
indicating the potential for neuroinvasion.5,6 Additionally, the isolation of
SARS-CoV-2 from the cerebrospinal fluid (CSF) in some patients further
supports the notion of neuroinvasion.7 Furthermore, numerous COVID-19
patients have reported anosmia (loss of smell) and various other
neurological symptoms, highlighting the neurological impact of the virus.8,9

Studies using human brain organoids have revealed clear evidence of
SARS-CoV-2 infection in cortical neurons, accompanied by metabolic
changes in infected and neighboring neurons.10 These studies have also
found the presence of ischemic damage and microinfarcts in post mortem
brain samples of COVID-19 patients, indicating the potential for severe
neurological consequences.11 In in-vivo studies using mice, similar to
previous reports of SARS-CoV, researchers observed increasing viral titers in
the brain following intranasal administration of SARS-CoV-2,
demonstrating the virus's neurotropic characteristics.12,13 Several
mechanisms of neuroinvasion have been proposed.

SARS-CoV-2 may directly infect vascular endothelial cells, potentially
allowing the virus to cross the blood-brain barrier (BBB).14 Another entry
route to the central nervous system (CNS) may involve the olfactory nerve,
where the virus can travel from the nasal passages to the brain.15 Damage to
lung blood vessels can lead to viral entry into the bloodstream, facilitating
spread to other organs, including the brain.16 Additionally, SARS-CoV-2
can induce systemic inflammatory responses, which have the potential to
disrupt the BBB and permit the virus or infected immune cells to reach the
brain.17 Furthermore, SARS-CoV-2 may utilize certain entry proteins

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expressed in the brain, such as ACE2, NRP1, and BSG, to facilitate its
invasion.18

To address this growing concern, strategies for early detection and
intervention are vital. Early detection involves monitoring COVID-19
patients for neurological symptoms like anosmia or ageusia.19,20 Using brain
organoids and in vivo models can help simulate and study the neuroinvasive
potential of the virus.21 For early intervention, research efforts should focus
on potential treatments that block the pathways SARS-CoV-2 uses to
invade the CNS. Exploring treatments that reduce inflammation or restore
the integrity of the BBB is crucial to prevent SARS-CoV-2 entry into the
brain.22,23 The efficacy of brain-penetrant antiviral drugs like Sofosbuvir in
treating SARS-CoV-2 CNS infection should be investigated.24 Further
study of ACE2, NRP1, and other receptors in the human brain is essential
for developing targeted interventions.25

Figure 2. Evidence of SARS-CoV-2 Invasion in Autopsy Samples. Autopsy Analysis
of (a) CoV antigen detected by anti-SARS-CoV protein antibodies (brown), (b)
SARS-CoV-2 RNA ISH showing intense signals in the mucus layer and cells (arrows) of
the epithelium, (c-f), Ultrastructural images of CoV-particles (c, arrows) attached to
kinocilia (c, white asterisks) and intracellular CoV particles (d-f), (f) high magnification of
CoV particles (black arrows).

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Figure 3. Potential Pathophysiological Mechanisms Underlying Cerebral Vascular
Involvement in COVID-19. A schematic representation of hypothesized mechanisms
linking COVID-19 to cerebral vascular damage, focusing on endothelial injury,
coagulopathy, and inflammation contributing to neurological manifestations.

4. Neuroprotective Strategies for Managing Neurological
Damage

Neurological damage mitigation is a complex and multifaceted endeavor,
necessitating a comprehensive approach that delves into diverse strategies
aimed at minimizing harm to the delicate nervous system. Among these
crucial strategies, three stand out prominently: the utilization of
anti-inflammatory drugs, the deployment of antiviral agents, and the
preservation of the blood-brain barrier

5. Strategies for Neurological Damage Mitigation

In the realm of neuroprotection, the role of anti-inflammatory drugs is
paramount, functioning as key players in the effort to minimize neuronal
damage. These drugs operate with precision by targeting the reduction of
inflammation, a critical factor in the pathophysiology of various
neurological complications. Specifically, their primary objective is to
down-regulate proinflammatory cytokines such as Interleukin-6 (IL-6) and
Tumor Necrosis Factor-alpha (TNF-α).26 This targeted approach aims to

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mitigate the severity of associated complications, emphasizing the
importance of managing inflammatory responses in the intricate landscape
of neurological health.

Another pivotal strategy in the arsenal against neurological challenges
involves the use of antiviral agents. These agents act as guardians by
inhibiting viral activity, a crucial aspect in the preservation of neurological
well-being. Their mechanisms extend beyond mere suppression,
encompassing the impediment of virus entry into the central nervous
system and the downregulation of virus receptors. By curbing viral activity,
these agents make significant strides in reducing neurotoxicity, fortifying the
defense against potential neurological damage.

The preservation of the blood-brain barrier emerges as a linchpin in the
safeguarding of neurological integrity. Functioning as a protective barricade,
this barrier regulates the passage of substances between the bloodstream and
the brain. The maintenance of this barrier is not only fundamental but also
integral in preventing neurological damage. A breach in this defense could
potentially expose the delicate neural environment to harmful agents,
emphasizing the critical role of a robust blood-brain barrier in neurological
health.

Within this intricate landscape, the exploration of Histone Deacetylase
Inhibitors (HDACi) emerges as a significant avenue.27 HDACi holds
promise in the amelioration of neurological damage through a multifaceted
approach. These inhibitors demonstrate efficacy by down-regulating
proinflammatory cytokines, thereby curbing the inflammatory response.
Additionally, HDACi plays a pivotal role in impeding virus entry and
replication within the central nervous system, adding another layer of
defense against potential neurological threats.

6. Ongoing Research and Clinical Trials for Novel
Therapeutic Solutions

The ongoing pursuit of effective interventions for managing and mitigating
neurological damage caused by viral infections is a dynamic field that

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continually expands through comprehensive clinical trials. These trials
encompass a diverse array of therapeutic options, ranging from traditional
pharmaceutical interventions to cutting-edge approaches like cell therapy.
In-depth exploration into convalescent plasma therapy, monoclonal
antibodies, immunoglobulin therapy, and cell therapy provides a nuanced
understanding of their potential efficacy in addressing neurological
complications arising from viral infections.28

Out of the ongoing clinical initiatives, approximately 86% focus on
examining the efficacy of small molecules or antibodies, either in isolation or
in conjunction with immunomodulators. The remaining approximately
14% of clinical endeavors are directed towards assessing vaccines and
therapies based on convalescent plasma to alleviate symptoms associated
with the disease.29

Vaccination, as a proactive measure against the spread of viruses with
neurological implications, remains a crucial focus. Emerging technologies,
such as nanoparticle vaccines, present a promising avenue. These vaccines,
designed to combine spike proteins from multiple coronaviruses, hold the
potential to offer broad protection against diverse strains. The exploration
of these innovative vaccination strategies adds a layer of anticipation to the
ongoing efforts in preventing and minimizing neurological complications
associated with viral infections.30

Furthermore, investigations into prominent drugs and therapies broaden
the spectrum of our understanding. Protease inhibitors, RNA-dependent
RNA polymerase inhibitors, immunomodulatory treatments, and
gene-editing techniques like CRISPR represent the frontier of antiviral
research.31 By targeting various aspects of viral infections, these
interventions aim to disrupt the replication and progression of viruses
within the body. A comprehensive grasp of the specifics of these trials,
including the drugs investigated and the precise aspects of viral infections
they address, enhances our comprehension and sets the stage for potential
breakthroughs in neuroprotection.

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7. Impact on Patient Care and Healthcare Systems

The exploration and application of prospective therapies hold immense
promise in significantly elevating the standard of patient care, presenting a
diversified arsenal of treatment options and preventive measures. The direct
targeting of neurological impacts stemming from viral infections through
these therapies marks a crucial advancement in the medical landscape.
However, a comprehensive understanding of the challenges that may arise
during the implementation of these interventions is imperative for a
nuanced approach to patient care enhancement.

Effective therapies not only promise to ameliorate the specific neurological
complications associated with viral infections but also have the potential to
address broader healthcare challenges. By reducing the severity and
incidence of these complications, these interventions could alleviate the
burden on healthcare systems. This, in turn, paves the way for more efficient
and streamlined patient care, fostering an environment where resources are
optimized, and healthcare professionals can focus on delivering
comprehensive and timely treatments.32

The public health implications of incorporating prospective therapies into
the broader healthcare framework are profound. The necessity of
widespread vaccination campaigns takes center stage, emphasizing the
importance of preventing the spread of viruses, particularly SARS-CoV-2,
which has demonstrated significant impacts on neurological health.
Concurrently, the establishment of early detection protocols emerges as a
critical strategy in mitigating the overall impact on public health.33

Addressing the challenges associated with implementing these therapies
becomes a focal point for healthcare systems aiming to optimize patient
care. By proactively tackling barriers to access, affordability, and
dissemination of these prospective therapies, healthcare systems can better
navigate the complexities of neurological health management. This holistic
approach not only benefits individual patients affected by viral infections
but also contributes to the overall resilience and adaptability of healthcare
infrastructures.34

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8. Conclusion

Navigating the Complex Terrain of SARS-CoV-2 Neurological
Impact

In the wake of the COVID-19 Pandemic, this comprehensive review has
ventured into the intricate landscape of neuroinvasive infections, focusing
on the unprecedented global impact and neurological consequences of the
SARS-CoV-2 pathogen. From exploring the multifaceted world of
neuroinvasion mechanisms to unraveling the evidence of neurological
damage, this journey has aimed to shed light on the complexities that define
the interplay between pathogens and the nervous system.

The significance of SARS-CoV-2’s global impact becomes increasingly
apparent as we navigate the neurological spectrum it presents, from mild
symptoms to severe conditions. The virus’s ability to infiltrate the central
nervous system adds layers of complexity to the ongoing battle against its
repercussions, urging researchers and clinicians to adapt and devise effective
therapeutic strategies.35

This review has highlighted the importance of robust therapeutic
interventions that address the diverse manifestations of neurological damage
caused by SARS-CoV-2. Strategies for early detection and intervention have
been highlighted as key components in mitigating the severity of
neurological consequences, The evidence of neuroinvasion, gleaned from
autopsy analyses, human brain organoids, and in vivo studies, forms a
foundation for future research directions and targeted interventions.

As we navigate the intricate terrain of SARS-CoV-2’s impact on the nervous
system, the pursuit of effective therapeutic solutions is emphasized.
Ongoing research and clinical trials offer hope to explore novel approaches
ranging from traditional pharmaceutical methods to cutting-edge
techniques, like cell therapy. The dynamic field of neuroprotection
continues to expand, providing a nuanced understanding of potential
breakthroughs in managing and mitigating neurological damage caused by
viral infections.

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As we stand at the intersection of scientific inquiry and practical
application, this review propels us forward into a future where adaptability,
resilience, and comprehensive understanding pave the way for
advancements in neuroinvasive pathogenic research. The journey to unravel
the mysteries of SARS-CoV-2 continues and will be guided by the collective
efforts of the scientific community in the pursuit of relief and hope for
those affected by the consequences of COVID-19.

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