The Mechanisms of Neuronal Damage in Virus Infections of the Nervous System

2020 ◽  
Vol 21 (15) ◽  
pp. 5475 ◽  
Author(s):  
Manuela Pennisi ◽  
Giuseppe Lanza ◽  
Luca Falzone ◽  
Francesco Fisicaro ◽  
Raffaele Ferri ◽  
...  

Increasing evidence suggests that Severe Acute Respiratory Syndrome-coronavirus-2 (SARS-CoV-2) can also invade the central nervous system (CNS). However, findings available on its neurological manifestations and their pathogenic mechanisms have not yet been systematically addressed. A literature search on neurological complications reported in patients with COVID-19 until June 2020 produced a total of 23 studies. Overall, these papers report that patients may exhibit a wide range of neurological manifestations, including encephalopathy, encephalitis, seizures, cerebrovascular events, acute polyneuropathy, headache, hypogeusia, and hyposmia, as well as some non-specific symptoms. Whether these features can be an indirect and unspecific consequence of the pulmonary disease or a generalized inflammatory state on the CNS remains to be determined; also, they may rather reflect direct SARS-CoV-2-related neuronal damage. Hematogenous versus transsynaptic propagation, the role of the angiotensin II converting enzyme receptor-2, the spread across the blood-brain barrier, the impact of the hyperimmune response (the so-called “cytokine storm”), and the possibility of virus persistence within some CNS resident cells are still debated. The different levels and severity of neurotropism and neurovirulence in patients with COVID-19 might be explained by a combination of viral and host factors and by their interaction.


2009 ◽  
Vol 62 (9-10) ◽  
pp. 461-467
Author(s):  
Ljiljana Nesic ◽  
Predrag Canovic ◽  
Zeljko Mijailovic ◽  
Jelena Djokovic

Introduction. Although well protected, brain is not resistant to infection agents. Acute infections of our nervous system appear more often in children and in persons who have medical history data about previous disorders, especially disorders of the nervous system. It is difficult to list possible risk factors which can be responsible for the appearance of infections of CNS and the resulting conditions. It is often difficult or impossible to determine what previous neural damage was (trauma, anoxic damages etc.) from those appearing during infections of CNS. All-inclusive anamnestic research reduces the possibility of approximate judgments. Material and methods. The research was based on the retrospective analysis of medical documentation of 275 patients. All patients were divided into three groups according to the final diagnosis. The first group consisted of 125 patients who were treated for acute virus encephalitis, the second group consisted of 125 patients who were treated for acute bacterial meningoencephalitis and the third group consisted of 25 patients who were treated for cerebritis. Discussion. In our studies sample, the youngest patient was 3 years old and the oldest was 87 years old. The highest number of patients with virus infection of the CNS was in the group under 25 years of age (45.6%). The highest number of patients with bacterial infections of the CNS and cerebritis was in the group of patients over 45 years of age (64%, 37%). Conclusion. Risk factors were more present in bacterial infections of the nervous system and cerebrit thanin virus infection of CNS. In virus infections of the CNS, 28% of patients had some risk factor, most often-chronic ethylism, diabetes mellitus and acquired heart diseases. In bacterial infections of the CNS, 64% of patients had some predisposed factor. The most frequent factor of risk in these patients were chronic otitis (21.6%) and craniotrauma (14.4%). In cerebritis, risk factors were present in 76% of patients and they were: sepsis (20%), chronic otitis (12%) and systemic lupus erythematosus (8%).


1946 ◽  
Vol 84 (4) ◽  
pp. 277-292 ◽  
Author(s):  
S. Edward Sulkin ◽  
Christine Zarafonetis ◽  
Andres Goth

Anesthesia with diethyl ether significantly alters the course and outcome of experimental infections with the equine encephalomyelitis virus (Eastern or Western type) or with the St. Louis encephalitis virus. No comparable effect is observed in experimental infections produced with rabies or poliomyelitis (Lansing) viruses. The neurotropic virus infections altered by ether anesthesia are those caused by viruses which are destroyed in vitro by this anesthetic, and those infections not affected by ether anesthesia are caused by viruses which apparently are not destroyed by ether in vitro. Another striking difference between these two groups of viruses is their pathogenesis in the animal host; those which are inhibited in vivo by ether anesthesia tend to infect cells of the cortex, basal ganglia, and only occasionally the cervical region of the cord. On the other hand, those which are not inhibited in vivo by ether anesthesia tend to involve cells of the lower central nervous system and in the case of rabies, peripheral nerves. This difference is of considerable importance in view of the fact that anesthetics affect cells of the lower central nervous system only in very high concentrations. It is obvious from the complexity of the problem that no clear-cut statement can be made at this point as to the mechanism of the observed effect of ether anesthesia in reducing the mortality rate in certain of the experimental neurotropic virus infections. Important possibilities include a direct specific effect of diethyl ether upon the virus and a less direct effect of the anesthetic upon the virus through its alteration of the metabolism of the host cell.


Neuropeptides ◽  
2006 ◽  
Vol 40 (6) ◽  
pp. 437
Author(s):  
E. Weihe ◽  
M. Bette ◽  
M.A.R. Preuss ◽  
M. Faber ◽  
M.K. Schäfer ◽  
...  

2013 ◽  
Vol 13 (4) ◽  
pp. 379-393 ◽  
Author(s):  
Orkide O. Koyuncu ◽  
Ian B. Hogue ◽  
Lynn W. Enquist

2015 ◽  
Author(s):  
Francisco González-Scarano

Several central nervous system diseases whose common elements include a long incubation period and a progressive clinical course were once called slow virus infections, because most of them are in fact caused by viruses. However, one group of these CNS diseases is now believed to be caused by abnormally configured proteins known as prions; rather than an etiologic designation, therefore, on the whole these diseases are better characterized by their chronicity, their transmissibility, and at this point, their inexorably deteriorating natural history. This chapter reviews the more common of these: HIV-associated dementia (HAD or HIVD), human T cell lymphotropic virus type 1 (HTLV-1)-associated myelopathy, Creutzfeldt-Jakob disease (CJD), progressive multifocal leukoencephalopathy (PML), and subacute sclerosing encephalitis (SSPE), which is associated with a variant of measles virus. Figures illustrate the pathogenesis and the pathology of HIV dementia, propagation of scrapie prion protein (PrP) in brain neurons, and spongiform brain changes of CJD. Tables list the stages of HAD and the clinical and pathologic characteristics distinguishing classic CJD and varient CJD. This module contains ­5 highly rendered figures, 2 tables, 57 references, and 5 MCQs. 


Sign in / Sign up

Export Citation Format

Share Document