Neurologic alterations due to respiratory virus infections
Open accessAbstract
Central Nervous System (CNS) infections are one of the most critical problems in public health, as frequently patients exhibit neurologic sequelae. Usually, CNS pathologies are caused by known neurotropic viruses such as measles virus (MV), herpes virus and human immunodeficiency virus (HIV), among others. However, nowadays respiratory viruses have placed themselves as relevant agents responsible for CNS pathologies. Among these neuropathological viruses are the human respiratory syncytial virus (hRSV), the influenza virus (IV), the coronavirus (CoV) and the human metapneumovirus (hMPV). These viral agents are leading causes of acute respiratory infections every year affecting mainly children under 5 years old and also the elderly. Up to date, several reports have described the association between respiratory viral infections with neurological symptoms. The most frequent clinical manifestations described in these patients are febrile or afebrile seizures, status epilepticus, encephalopathies and encephalitis. All these viruses have been found in cerebrospinal fluid (CSF), which suggests that all these pathogens, once in the lungs, can spread throughout the body and eventually reach the CNS. The current knowledge about the mechanisms and routes used by these neuro-invasive viruses remains scarce. In this review article, we describe the most recent findings associated to neurologic complications, along with data about the possible invasion routes of these viruses in humans and their various effects on the CNS, as studied in animal models.
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Respiratory viral diseases are associated with both acute and long-lasting psychopathological consequences in survivors.
“Respiratory viral diseases are associated with both acute and long-lasting psychopathological consequences in the survivors (Bohmwald et al., 2018).”
From Anxiety and depression in COVID-19 survivors: role of inflammatory and clinical predictors (2020) · cites this paper as Bohmwald et al., 2018
After CoV infects nasal cells, it can reach the entire brain and cerebrospinal fluid through the olfactory nerve and olfactory bulb within 7 days and cause inflammation and demyelinating reaction.
“For example, after CoV infects nasal cells, it can reach the entire brain and cerebrospinal fluid through the olfactory nerve and olfactory bulb within 7 days and cause inflammation and demyelinating reaction.”
From Nervous system involvement after infection with COVID-19 and other coronaviruses (2020) · cites this paper as Bohmwald et al., 2018
Removal of the olfactory bulb in mice resulted in restricted invasion of CoV into the CNS.
“However, removal of the olfactory bulb in the mice, resulted in a restricted invasion of CoV into the CNS (Bohmwald et al., 2018).”
From Nervous system involvement after infection with COVID-19 and other coronaviruses (2020) · cites this paper as Bohmwald et al., 2018
Primary glial cells cultured in vitro secrete a large amount of inflammatory factors such as IL-6, IL-12, IL-15, and TNF-α after being infected with CoV.
“Additionally, experiments have confirmed that primary glial cells cultured in vitro secrete a large amount of inflammatory factors such as IL-6, IL-12, IL-15, and TNF-α after being infected with CoV (Bohmwald et al., 2018).”
From Nervous system involvement after infection with COVID-19 and other coronaviruses (2020) · cites this paper as Bohmwald et al., 2018
Many viruses, including coronaviruses, propagate from nasal epithelium past cribriform plate to infect olfactory bulb; this central infection has been suggested to mediate olfactory deficits even without lasting olfactory epithelium damage.
“Many viruses, including coronaviruses, have been shown to propagate from the nasal epithelium past the cribriform plate to infect the OB; this form of central infection has been suggested to mediate olfactory deficits, even in the absence of lasting OE damage (60-65).”
From Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia (2020) · cites this paper as [60]
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- Authors
- Bohmwald, K., Gálvez, N. M. S., Ríos, M., & Kalergis, A. M.
- Affiliations
- Pontificia Universidad Católica de Chile (CL)
- Corresponding author
- Kalergis, Alexis M.
- Venue
- Frontiers in Cellular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2018-10-26
- Volume
- 12
- Pages
- 386-386
- ISSN
- 1662-5102 (ISSN-L)
- PMC
- PMC6212673
- OpenAlex
- W2898372989
- Cited by
- 636
- References
- 138
- Citations by year
- 2026: 21 · 2025: 22 · 2024: 38 · 2023: 75 · 2022: 101 · 2021: 169 · 2020: 203 · 2019: 4 · 2017: 1
- FWCI
- 13.79
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Cellular Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Instituto Milenio en Inmunología e Inmunoterapia (P09/016-F, 3180570, 1150862)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Infectious Encephalopathies and Encephalitis
- Health Sciences › Medicine › Epidemiology › Respiratory viral infections research
- Health Sciences › Medicine › Epidemiology › Virology and Viral Diseases
- Keywords
- respiratory viral infections, neurological complications, central nervous system infection, respiratory syncytial virus, influenza virus, coronavirus, human metapneumovirus, encephalitis, encephalopathy, status epilepticus, febrile seizures, cerebrospinal fluid, neurotropism, pediatric respiratory infection
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