The roles of Eph receptors, neuropilin-1, P2X7, and CD147 in COVID-19-associated neurodegenerative diseases: inflammasome and JaK inhibitors as potential promising therapies

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Abstract

The novel coronavirus disease 2019 (COVID-19) pandemic has spread worldwide, and finding a safe therapeutic strategy and effective vaccine is critical to overcoming severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Therefore, elucidation of pathogenesis mechanisms, especially entry routes of SARS-CoV-2 may help propose antiviral drugs and novel vaccines. Several receptors have been demonstrated for the interaction of spike (S) protein of SARS-CoV-2 with host cells, including angiotensin-converting enzyme (ACE2), ephrin ligands and Eph receptors, neuropilin 1 (NRP-1), P2X7, and CD147. The expression of these entry receptors in the central nervous system (CNS) may make the CNS prone to SARS-CoV-2 invasion, leading to neurodegenerative diseases. The present review provides potential pathological mechanisms of SARS-CoV-2 infection in the CNS, including entry receptors and cytokines involved in neuroinflammatory conditions. Moreover, it explains several neurodegenerative disorders associated with COVID-19. Finally, we suggest inflammasome and JaK inhibitors as potential therapeutic strategies for neurodegenerative diseases.

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Neurologic Manifestations of Hospitalized Patients With Coronavirus Disease 2019 in Wuhan, China

Ling Mao, Huijuan Jin, Mengdie Wang … (2020)

The outbreak of coronavirus disease 2019 (COVID-19) in Wuhan, China, is serious and has the potential to become an epidemic worldwide. Several studies have described typical clinical manifestations including fever, cough, diarrhea, and fatigue. However, to our knowledge, it has not been reported that patients with COVID-19 had any neurologic manifestations.

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Nowcasting and forecasting the potential domestic and international spread of the 2019-nCoV outbreak originating in Wuhan, China: a modelling study

Joseph Wu, Kathy Leung, Gabriel Leung (2020)

Summary Background Since Dec 31, 2019, the Chinese city of Wuhan has reported an outbreak of atypical pneumonia caused by the 2019 novel coronavirus (2019-nCoV). Cases have been exported to other Chinese cities, as well as internationally, threatening to trigger a global outbreak. Here, we provide an estimate of the size of the epidemic in Wuhan on the basis of the number of cases exported from Wuhan to cities outside mainland China and forecast the extent of the domestic and global public health risks of epidemics, accounting for social and non-pharmaceutical prevention interventions. Methods We used data from Dec 31, 2019, to Jan 28, 2020, on the number of cases exported from Wuhan internationally (known days of symptom onset from Dec 25, 2019, to Jan 19, 2020) to infer the number of infections in Wuhan from Dec 1, 2019, to Jan 25, 2020. Cases exported domestically were then estimated. We forecasted the national and global spread of 2019-nCoV, accounting for the effect of the metropolitan-wide quarantine of Wuhan and surrounding cities, which began Jan 23–24, 2020. We used data on monthly flight bookings from the Official Aviation Guide and data on human mobility across more than 300 prefecture-level cities in mainland China from the Tencent database. Data on confirmed cases were obtained from the reports published by the Chinese Center for Disease Control and Prevention. Serial interval estimates were based on previous studies of severe acute respiratory syndrome coronavirus (SARS-CoV). A susceptible-exposed-infectious-recovered metapopulation model was used to simulate the epidemics across all major cities in China. The basic reproductive number was estimated using Markov Chain Monte Carlo methods and presented using the resulting posterior mean and 95% credibile interval (CrI). Findings In our baseline scenario, we estimated that the basic reproductive number for 2019-nCoV was 2·68 (95% CrI 2·47–2·86) and that 75 815 individuals (95% CrI 37 304–130 330) have been infected in Wuhan as of Jan 25, 2020. The epidemic doubling time was 6·4 days (95% CrI 5·8–7·1). We estimated that in the baseline scenario, Chongqing, Beijing, Shanghai, Guangzhou, and Shenzhen had imported 461 (95% CrI 227–805), 113 (57–193), 98 (49–168), 111 (56–191), and 80 (40–139) infections from Wuhan, respectively. If the transmissibility of 2019-nCoV were similar everywhere domestically and over time, we inferred that epidemics are already growing exponentially in multiple major cities of China with a lag time behind the Wuhan outbreak of about 1–2 weeks. Interpretation Given that 2019-nCoV is no longer contained within Wuhan, other major Chinese cities are probably sustaining localised outbreaks. Large cities overseas with close transport links to China could also become outbreak epicentres, unless substantial public health interventions at both the population and personal levels are implemented immediately. Independent self-sustaining outbreaks in major cities globally could become inevitable because of substantial exportation of presymptomatic cases and in the absence of large-scale public health interventions. Preparedness plans and mitigation interventions should be readied for quick deployment globally. Funding Health and Medical Research Fund (Hong Kong, China).

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Neuroinflammation in Alzheimer's disease.

Michael T Heneka, Monica Carson, Joseph El Khoury … (2015)

Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease. Copyright © 2015 Elsevier Ltd. All rights reserved.

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Author and article information

Contributors

Farhad Seif:

ORCID: http://orcid.org/0000-0003-1275-2157

farhad.seif@outlook.com

Journal

Journal ID (nlm-ta): Cell Mol Biol Lett

Journal ID (iso-abbrev): Cell Mol Biol Lett

Title: Cellular & Molecular Biology Letters

Publisher: BioMed Central (London )

ISSN (Print): 1425-8153

ISSN (Electronic): 1689-1392

Publication date (Electronic): 2 February 2022

Publication date PMC-release: 2 February 2022

Publication date Collection: 2022

Volume: 27

Electronic Location Identifier: 10

Affiliations

[1 ]GRID grid.489440.5, ISNI 0000 0004 8033 4202, American Association of Kidney Patients, ; Tampa, FL USA

[2 ]GRID grid.411746.1, ISNI 0000 0004 4911 7066, Neuroscience Research Center, , Iran University of Medical Sciences, ; Tehran, Iran

[3 ]GRID grid.412571.4, ISNI 0000 0000 8819 4698, Shiraz Neuroscience Research Center, , Shiraz University of Medical Sciences, ; Shiraz, Iran

[4 ]GRID grid.510410.1, ISNI 0000 0004 8010 4431, Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), , Universal Scientific Education and Research Network (USERN), ; Tehran, Iran

[5 ]GRID grid.444768.d, ISNI 0000 0004 0612 1049, Department of Laboratory Sciences, School of Paramedical Sciences, , Kashan University of Medical Sciences, ; Kashan, Iran

[6 ]GRID grid.411746.1, ISNI 0000 0004 4911 7066, Rajaei Cardiovascular Medical and Research Center, , Iran University of Medical Sciences, ; Tehran, Iran

[7 ]GRID grid.412266.5, ISNI 0000 0001 1781 3962, Immunology Department, Faculty of Medicine, , Tarbiat Modares University, ; Tehran, Iran

[8 ]GRID grid.410443.6, ISNI 0000 0004 0370 3414, Department of Oncology, School of Medicine, , University of Maryland, ; Maryland, USA

[9 ]GRID grid.411746.1, ISNI 0000 0004 4911 7066, Department of Immunology, School of Medicine, , Iran University of Medical Sciences, ; Iran, Iran

[10 ]GRID grid.411705.6, ISNI 0000 0001 0166 0922, Endocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, , Tehran University of Medical Sciences, ; Tehran, Iran

[11 ]GRID grid.417689.5, Department of Immunology and Allergy, , Academic Center for Education, Culture, and Research (ACECR), ; Enghelab St., Aboureyhan St., Vahid Nazari Crossroad, P17, 1315795613 Tehran, Iran

Author information

Farhad Seif http://orcid.org/0000-0003-1275-2157

Article

Publisher ID: 311

DOI: 10.1186/s11658-022-00311-1

PMC ID: 8809072

PubMed ID: 35109786

SO-VID: 10a503e1-89db-43a9-afda-dfb83be84b66

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

History

Date received : 13 December 2021

Date accepted : 14 January 2022

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Keywords: covid-19,cns,ephrin,neuropilin-1,p2x7,cd147,cytokine,jak,inflammasome,neurodegenerative diseases,alzheimer’s disease,parkinson’s disease

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Keywords: covid-19, cns, ephrin, neuropilin-1, p2x7, cd147, cytokine, jak, inflammasome, neurodegenerative diseases, alzheimer’s disease, parkinson’s disease

The roles of Eph receptors, neuropilin-1, P2X7, and CD147 in COVID-19-associated neurodegenerative diseases: inflammasome and JaK inhibitors as potential promising therapies

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Novel Coronavirus Disease COVID-19

Most cited references 161

Neurologic Manifestations of Hospitalized Patients With Coronavirus Disease 2019 in Wuhan, China

Nowcasting and forecasting the potential domestic and international spread of the 2019-nCoV outbreak originating in Wuhan, China: a modelling study

Neuroinflammation in Alzheimer's disease.

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