scholarly journals A Review of Coronavirus Infection in the Central Nervous System of Cats and Mice

2001 ◽  
Vol 15 (5) ◽  
pp. 438-444 ◽  
Author(s):  
Janet E. Foley ◽  
Christian Leutenegger
2021 ◽  
Vol 40 (4) ◽  
pp. 33-42
Author(s):  
Igor V. Litvinenko ◽  
Miroslav M. Odinak ◽  
Nikolay V. Tsygan ◽  
Aleksander V. Ryabtsev

The central nervous system seems to be quite vulnerable to SARS-CoV-2, leading to a variety of alteration pathways, high incidence and variability of the neurological symptoms of COVID-19. The COVID-19 symptoms, possibly associated with alteration to the central nervous system, include hyperthermia, shortness of breath, fatigue, headache, dizziness, dysphonia, dysphagia, hyposmia and anosmia, hypogeusia and ageusia, impairment of consciousness. The impairment of olfaction and gustation are the most common symptoms of the nervous system alteration (98% and 70%, respectively), which is most likely a consequence of the alteration of the receptors. Presumably the pathogenesis of dysphonia and dysphagia may involve neurodegenerative mechanisms or may be associated with a predominantly demyelinating alteration of the caudal cranial nerves. Pathomorphological findings in the brain of the COVID-19 patients include diffuse hypoxic and focal ischemic injuries of various sizes up to ischemic infarctions (in thrombosis of large arteries); microangiopathy; vasculitis; diapedetic and confluent hemorrhages with possible progression to hemorrhagic infarctions and rarely intracerebral hematomas. Acute cerebrovascular accident worsens the course of COVID-19 and can worsen the clinical outcome, taking into account the mechanisms of the central nervous system alteration in highly contagious coronavirus infections (SARS-CoV, MERS, SARS-CoV-2), including embolism, hypoxia, neurodegeneration, systemic inflammatory response and immune-mediated alteartion to the nervous tissue. A fairly rare complication of coronavirus infection, however, acute myelitis requires attention due to the severity of neurological disorders. The literature data show high incidence and polymorphism of the symptoms of the central nervous system alteration, as well as the important role of the cerebrovascular and neurodegenerative pathogenesis of brain alteration in COVID-19, which is taken into account in examining and treating the patients with new coronavirus infection. (1 figure, bibliography: 61 refs)


2006 ◽  
Vol 4 (2) ◽  
pp. 121-132 ◽  
Author(s):  
Cornelia C. Bergmann ◽  
Thomas E. Lane ◽  
Stephen A. Stohlman

2008 ◽  
Vol 21 (2) ◽  
pp. 173-188 ◽  
Author(s):  
Katherine S. Held ◽  
William G. Glass ◽  
Yevgeniya I. Orlovsky ◽  
Kimberly A. Shamberger ◽  
Ted D. Petley ◽  
...  

2010 ◽  
Vol 84 (21) ◽  
pp. 11030-11044 ◽  
Author(s):  
Susan J. Bender ◽  
Judith M. Phillips ◽  
Erin P. Scott ◽  
Susan R. Weiss

ABSTRACT Coronavirus infection of the murine central nervous system (CNS) provides a model for studies of viral encephalitis and demyelinating disease. Mouse hepatitis virus (MHV) neurotropism varies by strain: MHV-A59 causes mild encephalomyelitis and demyelination, while the highly neurovirulent strain JHM.SD (MHV-4) causes fatal encephalitis with extensive neuronal spread of virus. In addition, while neurons are the predominant CNS cell type infected in vivo, the canonical receptor for MHV, the carcinoembryonic antigen family member CEACAM1a, has been demonstrated only on endothelial cells and microglia. In order to investigate whether CEACAM1a is also expressed in other cell types, ceacam1a mRNA expression was quantified in murine tissues and primary cells. As expected, among CNS cell types, microglia expressed the highest levels of ceacam1a, but lower levels were also detected in oligodendrocytes, astrocytes, and neurons. Given the low levels of neuronal expression of ceacam1a, primary neurons from wild-type and ceacam1a knockout mice were inoculated with MHV to determine the extent to which CEACAM1a-independent infection might contribute to CNS infection. While both A59 and JHM.SD infected small numbers of ceacam1a knockout neurons, only JHM.SD spread efficiently to adjacent cells in the absence of CEACAM1a. Quantification of mRNA for the ceacam1a-related genes ceacam2 and psg16 (bCEA), which encode proposed alternative MHV receptors, revealed low ceacam2 expression in microglia and oligodendrocytes and psg16 expression exclusively in neurons; however, only CEACAM2 mediated infection in human 293T cells. Therefore, neither CEACAM2 nor PSG16 is likely to be an MHV receptor on neurons, and the mechanism for CEACAM1a-independent neuronal spread of JHM.SD remains unknown.


Virology ◽  
2013 ◽  
Vol 447 (1-2) ◽  
pp. 112-120 ◽  
Author(s):  
Maria Teresa P. de Aquino ◽  
Shweta S. Puntambekar ◽  
Carine Savarin ◽  
Cornelia C. Bergmann ◽  
Timothy W. Phares ◽  
...  

Glia ◽  
2020 ◽  
Author(s):  
Vrushali Mangale ◽  
Amber R. Syage ◽  
H. Atakan Ekiz ◽  
Dominic D. Skinner ◽  
Yuting Cheng ◽  
...  

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