scholarly journals COVID-19 Is Changing Our Understanding of the Neuroscience of Viral Infections: What We Can Do to Prepare for the Future?

2022 ◽  
Vol 14 (1) ◽  
pp. 89-89
Author(s):  
Kore Kai Liow ◽  
Jason Viereck

In the approximately two years since the emergence of COVID-19 (Coronavirus Disease 2019) myriad neurological symptoms have been reported that are seemingly unrelated to each other [...]

2021 ◽  
Vol 36 (4) ◽  
pp. 285-296
Author(s):  
Adriana Wawer ◽  
Agnieszka Piechal

Objective. Some viral infections can have a harmful effect on the functioning of the nervous system and can even cause serious neurological damage. This work aims to review the results of studies published so far concerning neurological complications in people infected with coronaviruses, especially SARS-CoV-2, and possible mechanisms responsible for nervous system damage. Literature review. Recently, there have been reports that coronaviruses, including SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), cause acute respiratory disease, exhibit neurotropic properties and can also cause neurological symptoms. There are studies published showing that these viruses may penetrate to the brain and cerebrospinal fluid. Conclusions. Coronaviruses are still poorly understood, so it seems important to study the potential impact of SARS-CoV-2 infections on the nervous system. It seems appropriate that patients infected with SARS-CoV-2 should be early evaluated for neurological symptoms, including headache and impaired consciousness.


2020 ◽  
Vol 94 (22) ◽  
Author(s):  
Yujun Li ◽  
Haimin Wang ◽  
Xiaojuan Tang ◽  
Shisong Fang ◽  
Danting Ma ◽  
...  

ABSTRACT The ongoing coronavirus disease 2019 (COVID-19) pandemic has caused >20 million infections and >750,000 deaths. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of COVID-19, has been found closely related to the bat coronavirus strain RaTG13 (Bat-CoV RaTG13) and a recently identified pangolin coronavirus (Pangolin-CoV-2020). Here, we first investigated the ability of SARS-CoV-2 and three related coronaviruses to utilize animal orthologs of angiotensin-converting enzyme 2 (ACE2) for cell entry. We found that ACE2 orthologs of a wide range of domestic and wild mammals, including camels, cattle, horses, goats, sheep, cats, rabbits, and pangolins, were able to support cell entry of SARS-CoV-2, suggesting that these species might be able to harbor and spread this virus. In addition, the pangolin and bat coronaviruses, Pangolin-CoV-2020 and Bat-CoV RaTG13, were also found able to utilize human ACE2 and a number of animal-ACE2 orthologs for cell entry, indicating risks of spillover of these viruses into humans in the future. We then developed potently anticoronavirus ACE2-Ig proteins that are broadly effective against the four distinct coronaviruses. In particular, through truncating ACE2 at its residue 740 but not 615, introducing a D30E mutation, and adopting an antibody-like tetrameric-ACE2 configuration, we generated an ACE2-Ig variant that neutralizes SARS-CoV-2 at picomolar range. These data demonstrate that the improved ACE2-Ig variants developed in this study could potentially be developed to protect from SARS-CoV-2 and some other SARS-like viruses that might spillover into humans in the future. IMPORTANCE The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent of the currently uncontrolled coronavirus disease 2019 (COVID-19) pandemic. It is important to study the host range of SARS-CoV-2, because some domestic species might harbor the virus and transmit it back to humans. In addition, insight into the ability of SARS-CoV-2 and SARS-like viruses to utilize animal orthologs of the SARS-CoV-2 receptor ACE2 might provide structural insight into improving ACE2-based viral entry inhibitors. In this study, we found that ACE2 orthologs of a wide range of domestic and wild animals can support cell entry of SARS-CoV-2 and three related coronaviruses, providing insights into identifying animal hosts of these viruses. We also developed recombinant ACE2-Ig proteins that are able to potently block these viral infections, providing a promising approach to developing antiviral proteins broadly effective against these distinct coronaviruses.


Author(s):  
Myriam Herrnberger ◽  
Nadine Durmazel ◽  
Frank Birklein

Abstract Neurological symptoms might be associated with a Covid-19 infection. There are frequent reports in the last weeks. The neurological symptoms range from harmless side effects of a viral infection to meningoencephalitis and acute haemorrhagic necrotizing encephalopathy.Our patient reported burning headache and paresthesia as the initial symptoms mainly without other signs of viral infection like cough or fever. Such an initial neurological presentation seems to be rare. Most cases have neurological symptoms which can be expected after severe systemic viral infections like fever associated headache. Many COVID-19 patients with mild disease are at home and the further course is unknown. Our case shows, that neurological symptoms can be the first manifestation of an COVID-19 disease. While restricted paraesthesia has been reported in SARS-CoV-2 infections, hemisymptoms have not been described as initial symptoms.


2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Saber Soltani ◽  
Alireza Tabibzadeh ◽  
Armin Zakeri ◽  
Amir Mohammad Zakeri ◽  
Tayebeh Latifi ◽  
...  

Abstract The ongoing pandemic of Coronavirus disease 2019 (COVID-19) has infected more than 27 million confirmed cases and 8,90,000 deaths all around the world. Verity of viral infections can infect the nervous system; these viral infections can present a wide range of manifestation. The aim of the current study was to systematically review the COVID-19 associated central nervous system manifestations, mental and neurological symptoms. For that we conducted a comprehensive systematic literature review of four online databases, including Web of Science, PubMed, Scopus and Embase. All relevant articles that reported psychiatric/psychological symptoms or disorders in COVID-19 without considering time and language restrictions were assessed. All the study procedures were performed based on the PRISMA criteria. Due to the screening, 14 studies were included. The current study result indicated that, the pooled prevalence of CNS or mental associated disorders with 95% CI was 50.68% (6.68–93.88). The most prevalence symptoms were hyposmia/anosmia/olfactory dysfunction (number of study: 10) with 36.20% (14.99–60.51). Only one study reported numbness/paresthesia and dysphonia. Pooled prevalence of numbness/paresthesia and dysphonia was 5.83% (2.17–12.25) and 2.39% (10.75–14.22). The pooled prevalence of depression and anxiety was 3.52% (2.62–4.54) and 13.92% (9.44–19.08). Our findings demonstrate that COVID-19 has a certain relation with neurological symptoms. The hypsomia, anosmia or olfactory dysfunction was most frequent symptom. Other symptoms were headache or dizziness, dysgeusia or ageusia, dysphonia and fatigue. Depression, anxiety, and confusion were less frequent symptoms.


2020 ◽  
Vol 14 (suppl 1) ◽  
pp. 725-731 ◽  
Author(s):  
Muhammad Bilal ◽  
Muhammad Imran Khan ◽  
Muhammad Shahzad Nazir ◽  
Ishtiaq Ahmed ◽  
Hafiz M.N. Iqbal

Despite the earlier two Coronavirus outbreaks, this appearance of the third Coronavirus outbreak has brought several complications and now emerged as a human-health related pandemic issue. The wide geographical spread and transmissibility of newly emerged novel-Coronavirus (2019-nCoV) and severity of coronavirus disease 2019 (COVID-19) raised serious concerns about the future trajectory of the 2019-nCoV/COVID-19 outbreak. Herein, we have briefly covered some important aspects of the 2019-nCoV/COVID-19 outbreak to highlight the need to learn lessons for a safer future. First, an epidemiological comparison of respiratory viral infections with particular reference to 2019-nCoV is given with relevant examples. Following that, considering the earlier two Coronavirus outbreaks, the emergence of another new 2019-nCoV is given. Finally, the lesson learned, so far, and key concerns for pandemic impact assessment at large and COVID-19, in particular, are discussed for future considerations.


2020 ◽  
Vol 13 (8) ◽  
pp. e237146
Author(s):  
Rita Figueiredo ◽  
Vera Falcão ◽  
Maria João Pinto ◽  
Carla Ramalho

Acute facial nerve disease leading to peripheral facial paralysis is commonly associated with viral infections. COVID-19 may be a potential cause of peripheral facial paralysis and neurological symptoms could be the first and only manifestation of the disease. We report a case of a term pregnancy diagnosed with COVID-19 after presenting with isolated peripheral facial palsy.


2020 ◽  
Author(s):  
Vatsalya Vatsalya ◽  
Fengyuan Li ◽  
Jane C Frimodig ◽  
Khushboo S Gala ◽  
Shweta Srivastava ◽  
...  

Introduction Emerging infectious diseases, especially the coronavirus disease identified in 2019 (COVID-19), can be complicated by a severe exacerbation in the Th17 cell-mediated IL-17 proinflammatory immune storm. This enhanced immune response plays a major role in mortality and morbidity, including neurological symptoms. We hypothesized that countering the cytokine storm with thiamine may have therapeutic efficacy in lowering the Th17 cell proinflammatory response. We used an in vitro study and corroborated those results in disease controls (DC). We developed an effective dose range and model for key pharmacokinetic measures with the potential of targeting the cytokine storm and neurological symptoms of COVID-19. Study Participants and Methods We investigated the effect of a three-week 200 mg dose of thiamine in lowering the Th17 response in sixteen DC (proinflammatory origin due to heavy alcohol drinking) patients; and eight healthy control/volunteers (HV) as a pilot clinical-translational investigation. To further investigate, we performed an in vitro study evaluating the effectiveness of thiamine treatment in lowering the Th17 proinflammatory response in a mouse macrophage cell line (RAW264.7) treated with ethanol. In this in vitro study, 100 mg/day equivalent (0.01 ug/ml) thiamine was used. Based on recent publications, we compared the results of the IL-17 response from our clinical and in vitro study to those found in other proinflammatory disease conditions (metabolic conditions, septic shock, viral infections and COVID-19), including symptoms, and dose ranges of effective and safe administration of thiamine. We developed a dose range and pharmacokinetic profile for thiamine as a novel intervention strategy in COVID-19 to alleviate the effects of the cytokine storm and neurological symptoms. Results The DC group showed significantly elevated proinflammatory cytokines compared to HV. Three-week of 200 mg daily thiamine treatment significantly lowered the baseline IL-17 levels while increased IL-22 levels (anti-inflammatory response). This was validated by an in vitro macrophage response using a lower thiamine dose equivalent (100 mg), which resulted in attenuation of IL-17 and elevation of IL-22 at the mRNA level compared to the ethanol-only treated group. In humans, a range of 79-474 mg daily of thiamine was estimated to be effective and safe as an intervention for the COVID-19 cytokine storm. A literature review showed that several neurological symptoms of COVID-19 (which exist in 45.5% of the severe cases) occur in other viral infections and neuroinflammatory states that may also respond to thiamine treatment. Discussion The Th17 mediated IL-17 proinflammatory response can potentially be attenuated by thiamine. Thiamine, a very safe drug even at very high doses, could be repurposed for treating the cytokine/immune storm of COVID-19 and the subsequent neurological symptoms observed in COVID-19 patients. Further studies using thiamine as an interventional/prevention strategy in severe COVID-19 patients could identify its precise anti-inflammatory role.


2021 ◽  
Vol 11 ◽  
Author(s):  
Vatsalya Vatsalya ◽  
Fengyuan Li ◽  
Jane Frimodig ◽  
Khushboo S. Gala ◽  
Shweta Srivastava ◽  
...  

Coronavirus disease identified in 2019 (COVID-19) can be complicated by the Th17 cell-mediated IL-17 proinflammatory response. We tested if thiamine can effectively lower the Th17 response in a clinical study [Proinflammatory state in alcohol use disorder patients termed as disease controls (DC)] and corroborated the results using an in vitro study. We developed an effective dose range and model for key pharmacokinetic measures with the potential of targeting the cytokine storm and neurological symptoms of COVID-19. Three-week 200 mg dose of thiamine was administered to sixteen DC patients. Eight healthy volunteers (HV) were also included in this investigation. A subsequent in vitro study was performed to validate the effectiveness of thiamine [100 mg/day equivalent (0.01 μg/ml)] treatment in lowering the Th17 proinflammatory response in a mouse macrophage cell line (RAW264.7) treated with ethanol. Based on recent publications, we compared the results of the IL-17 response from our clinical and in vitro study to those found in other proinflammatory disease conditions (metabolic conditions, septic shock, viral infections and COVID-19) and effective and safe dose ranges of thiamine. We developed a pharmacokinetic profile for thiamine dose range as a novel intervention strategy in COVID-19. DC group showed significantly elevated proinflammatory cytokines compared to HV. Thiamine-treated DC patients showed significant lowering in IL-17 and increase in the IL-22 levels. In humans, a range of 79–474 mg daily of thiamine was estimated to be effective and safe as an intervention for the COVID-19 cytokine storm. A literature review showed that several neurological symptoms of COVID-19 (∼45.5% of the severe cases) occur in other viral infections and neuroinflammatory states that may also respond to thiamine treatment. Thiamine, a very safe drug even at very high doses, could be repurposed for treating the Th17 mediated IL-17 immune storm, and the subsequent neurological symptoms observed in COVID-19. Further studies using thiamine as an intervention/prevention strategy in COVID-19 patients could identify its precise anti-inflammatory role.


2019 ◽  
Vol 13 (1) ◽  
pp. 59-63
Author(s):  
Maria Luisa Gastaldello ◽  
Marcello Bigliocca ◽  
Mauro Campanini

The present study illustrates two cases of Toxocara canis infection: a 77-year-old man presenting with bilateral uveitis, sepsis, and non-convulsive status epilepticus (patient A); and a 63-year-old woman with a history of treated breast cancer, presenting with sight loss and paralysis of the right eye, neurological symptoms, pulmonary embolism, pneumonia, and a post traumatic vertebral fracture (patient B). Both diagnoses were challenging because the acute comorbidities withdrew the attention from the actual cause of the disease, and in one case the steroid treatment possibly affected the laboratory indexes. The lack of response to antibiotics and the involvement of specific organs and districts suggested parasitic infection. Indeed, immunoblot assay revealed the presence of specific T. canis immunoglobulin G antibodies. Both patients improved with albendazole 800 mg/die (400 mg ×2) for 28 days; the neurological state normalized, while sight and eye motility remained impaired. Overall, the findings from these two toxocariasis cases indicate that the occurrence of severe neurological symptoms associated with ocular involvement should generate suspicion of parasitic infection rather than leading to differential diagnosis of common presentations such as bacterial and viral infections or autoimmune diseases.


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