Covid-19 Induced Neuroinflammation

Main Article Content

Rajen Dey

Abstract

The respiratory illness COVID-19 started a global pandemic in 2019 and continued until 2020. Globally, the epidemic claimed the lives of around 480,000 persons and affected 9.5 million people. SARS-CoV-2 is the primary cause of this outbreak. SARS-CoV-2 is an RNA virus that is encapsulated and can infect multiple organs. It can enter the host through spike proteins. This epidemic had a serious impact on the brain as well. The recovered patients experienced neurological problems following COVID-19, neuropsychiatric symptoms, cognitive impairment, and difficulty concentrating. Nonetheless, the primary cause of all these clinical disorders or changes in psycho-behavioral patterns is consistently neuroinflammation. The neurological characteristics of COVID-19 patients and the neuroinflammatory effects of SARS-CoV-2 infection will be the main topics of this review. Studies have indicated that the brain inflammation caused by COVID-19 may be partly attributed to the overproduction of free radicals such as ROS and NO as well as the downregulation of antioxidant enzymes. Furthermore, cytokine storm, which is brought on by inflammatory cytokines like IL-1β, IFN-γ, and IL-6, may be the cause of major depressive disorder (MDD). Thus, it is clear from this analysis how critical it is to manage the harmful neuroinflammatory effects of SARS-CoV-2 infection, which ultimately result in the death of neurons and neurological impairment. Considering all the information, it is possible to conclude that controlling these inflammatory effects effectively may be a useful tactic for preserving normal brain function.

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How to Cite
Rajen Dey. (2024). Covid-19 Induced Neuroinflammation. Journal of Advanced Zoology, 45(2), 1544–1548. https://doi.org/10.53555/jaz.v45i2.4447
Section
Articles
Author Biography

Rajen Dey

Department of Medical Laboratory Technology, School of Allied Health Sciences, Swami Vivekananda University, Telinipara, Barasat-Barrackpore Rd, Bara Kanthalia, West Bengal - 700121, India.

References

Gupta, A., Madhavan, M. V., Sehgal, K., Nair, N., Mahajan, S., Sehrawat, T. S., Bikdeli, B., Ahluwalia, N., Ausiello, J. C., Wan, E. Y., Freedberg, D. E., Kirtane, A. J., Parikh, S. A., Maurer, M. S., Nordvig, A. S., Accili, D., Bathon, J. M., Mohan, S., Bauer, K. A., Leon, M. B., … Landry, D. W. (2020). Extrapulmonary manifestations of COVID-19. Nature medicine, 26(7), 1017–1032.

Zou, X., Chen, K., Zou, J., Han, P., Hao, J., & Han, Z. (2020). Single-cell RNA-seq data analysis on the receptor ACE2 expression reveals the potential risk of different human organs vulnerable to 2019-nCoV infection. Frontiers of medicine, 14(2), 185–192.

Dong, E., Du, H., & Gardner, L. (2020). An interactive web-based dashboard to track COVID-19 in real time. The Lancet. Infectious diseases, 20(5), 533–534.

Hoffmann, M., Kleine-Weber, H., Schroeder, S., Krüger, N., Herrler, T., Erichsen, S., Schiergens, T. S., Herrler, G., Wu, N. H., Nitsche, A., Müller, M. A., Drosten, C., & Pöhlmann, S. (2020). SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor. Cell, 181(2), 271–280.e8.

Wiersinga, W. J., Rhodes, A., Cheng, A. C., Peacock, S. J., & Prescott, H. C. (2020). Pathophysiology, Transmission, Diagnosis, and Treatment of Coronavirus Disease 2019 (COVID-19): A Review. JAMA, 324(8), 782–793.

Balcom, E. F., Nath, A., & Power, C. (2021). Acute and chronic neurological disorders in COVID-19: potential mechanisms of disease. Brain: a journal of neurology, 144(12), 3576–3588.

Ahmad, I., & Rathore, F. A. (2020). Neurological manifestations and complications of COVID-19: A literature review. Journal of clinical neuroscience: official journal of the Neurosurgical Society of Australasia, 77, 8–12.

Mao, L., Jin, H., Wang, M., Hu, Y., Chen, S., He, Q., Chang, J., Hong, C., Zhou, Y., Wang, D., Miao, X., Li, Y., & Hu, B. (2020). Neurologic Manifestations of Hospitalized Patients With Coronavirus Disease 2019 in Wuhan, China. JAMA neurology, 77(6), 683–690.

Mehta, P., McAuley, D. F., Brown, M., Sanchez, E., Tattersall, R. S., Manson, J. J., & HLH Across Speciality Collaboration, UK (2020). COVID-19: consider cytokine storm syndromes and immunosuppression. Lancet (London, England), 395(10229), 1033–1034.

Niraula, A., Sheridan, J. F., & Godbout, J. P. (2017). Microglia Priming with Aging and Stress. Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology, 42(1), 318–333.

Klein, R. S., Garber, C., Funk, K. E., Salimi, H., Soung, A., Kanmogne, M., Manivasagam, S., Agner, S., & Cain, M. (2019). Neuroinflammation During RNA Viral Infections. Annual review of immunology, 37, 73–95.

Said, E. A., Tremblay, N., Al-Balushi, M. S., Al-Jabri, A. A., & Lamarre, D. (2018). Viruses Seen by Our Cells: The Role of Viral RNA Sensors. Journal of immunology research, 2018, 9480497.

Jensen, S., & Thomsen, A. R. (2012). Sensing of RNA viruses: a review of innate immune receptors involved in recognizing RNA virus invasion. Journal of virology, 86(6), 2900–2910.

Choudhury, A., & Mukherjee, S. (2020). In silico studies on the comparative characterization of the interactions of SARS-CoV-2 spike glycoprotein with ACE-2 receptor homologs and human TLRs. Journal of medical virology, 92(10), 2105–2113.

Aboudounya, M. M., & Heads, R. J. (2021). COVID-19 and Toll-Like Receptor 4 (TLR4): SARS-CoV-2 May Bind and Activate TLR4 to Increase ACE2 Expression, Facilitating Entry and Causing Hyperinflammation. Mediators of inflammation, 2021, 8874339.

Singh, M., Bansal, V., & Feschotte, C. (2020). A Single-Cell RNA Expression Map of Human Coronavirus Entry Factors. Cell reports, 32(12), 108175.

Dutta, D., Liu, J., & Xiong, H. (2022). NLRP3 inflammasome activation and SARS-CoV-2-mediated hyperinflammation, cytokine storm and neurological syndromes. International journal of physiology, pathophysiology and pharmacology, 14(3), 138–160.

Helms, J., Kremer, S., Merdji, H., Clere-Jehl, R., Schenck, M., Kummerlen, C., Collange, O., Boulay, C., Fafi-Kremer, S., Ohana, M., Anheim, M., & Meziani, F. (2020). Neurologic Features in Severe SARS-CoV-2 Infection. The New England journal of medicine, 382(23), 2268–2270.

Dayarathna, S., Jeewandara, C., Gomes, L., Somathilaka, G., Jayathilaka, D., Vimalachandran, V., Wijewickrama, A., Narangoda, E., Idampitiya, D., Ogg, G. S., & Malavige, G. N. (2020). Similarities and differences between the 'cytokine storms' in acute dengue and COVID-19. Scientific reports, 10(1), 19839.

Fontes-Dantas, F. L., Fernandes, G. G., Gutman, E. G., De Lima, E. V., Antonio, L. S., Hammerle, M. B., Mota-Araujo, H. P., Colodeti, L. C., Araújo, S. M. B., Froz, G. M., da Silva, T. N., Duarte, L. A., Salvio, A. L., Pires, K. L., Leon, L. A. A., Vasconcelos, C. C. F., Romão, L., Savio, L. E. B., Silva, J. L., da Costa, R., … Figueiredo, C. P. (2023). SARS-CoV-2 Spike protein induces TLR4-mediated long-term cognitive dysfunction recapitulating post-COVID-19 syndrome in mice. Cell reports, 42(3), 112189.

Zhou, Z., Kang, H., Li, S., & Zhao, X. (2020). Understanding the neurotropic characteristics of SARS-CoV-2: from neurological manifestations of COVID-19 to potential neurotropic mechanisms. Journal of neurology, 267(8), 2179–2184.

Camini, F. C., da Silva Caetano, C. C., Almeida, L. T., & de Brito Magalhães, C. L. (2017). Implications of oxidative stress on viral pathogenesis. Archives of virology, 162(4), 907–917.

Rincón, J., Correia, D., Arcaya, J. L., Finol, E., Fernández, A., Pérez, M., Yaguas, K., Talavera, E., Chávez, M., Summer, R., & Romero, F. (2015). Role of Angiotensin II type 1 receptor on renal NAD(P)H oxidase, oxidative stress and inflammation in nitric oxide inhibition induced-hypertension. Life sciences, 124, 81–90.

Popa-Wagner, A., Mitran, S., Sivanesan, S., Chang, E., & Buga, A. M. (2013). ROS and brain diseases: the good, the bad, and the ugly. Oxidative medicine and cellular longevity, 2013, 963520.