SARS-CoV-2 İlişkili Pediatrik Ensefalit Olgusu

Abstract

COVID-19'a neden olan SARS-CoV-2, insan hücrelerini enfekte etmek için anjiyotensin dönüştürücü enzim 2 (ACE-2) reseptörüne bağlanır. Beyindeki glial hücreler ve nöronlar; ACE-2 reseptörü içerdiğinden dolayı SARS-CoV-2'nin potansiyel hedeflerindendir. Bu durum SARS-CoV-2’ye nörotrofik bir özellik sağlar. Ensefalit, enfeksiyonun veya vücudun immün savunmasının neden olduğu beyin parankiminin inflamasyonu olarak tanımlanır. Bu yazıda değerlendirmeler sonucunda SARS-CoV-2 ile ilişkili olabileceği düşünülen, bilinç kaybı ve tepkisizlik ile getirilen ensefalit olgusu sunuldu.

Keywords

• COVID-19
• ensefalit
• nörotrofik
• SARS-CoV-2

A Case of SARS-CoV-2 Associated Pediatric Encephalitis

Abstract

SARS-CoV-2, which causes COVID-19, binds to the angiotensin-converting enzyme 2 (ACE-2) receptor to infect human cells. Glial cells, and neurons in the brain have been reported to contain ACE-2 receptors, making them potential targets of SARS-CoV-2. This provides neurotrophic properties to the SARS-CoV-2. Encephalitis is defined as inflammation of the brain parenchyma caused by an infection or the body's immune defenses. In this article, we present a case of encephalitis, which was brought with cognitive impairment and decreased responsiveness, which may be associated with SARS-CoV-2 as a result of the evaluations.

Keywords

• COVID-19
• encephalitis
• neurotrophic
• SARS-CoV-2

References

1. 1. Gómez CE, Perdiguero B, Esteban M. Emerging SARS-CoV-2 Variants and Impact in Global Vaccination Programs against SARS-CoV-2/COVID-19. Vaccines (Basel). 2021;9. doi:10.3390/vaccines9030243
2. 2. Lu R, Zhao X, Li J, Niu P, Yang B, Wu H, et al. Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. Lancet. 2020;395: 565–574.
3. 3. Zhou Z, Kang H, Li S, Zhao X. Understanding the neurotropic characteristics of SARS-CoV-2: from neurological manifestations of COVID-19 to potential neurotropic mechanisms. J Neurol. 2020;267: 2179–2184.
4. 4. Solomon T, Michael BD, Smith PE, Sanderson F, Davies NWS, Hart IJ, et al. Management of suspected viral encephalitis in adults – Association of British Neurologists and British Infection Association National Guidelines. Journal of Infection. 2012. pp. 347–373. doi:10.1016/j.jinf.2011.11.014
5. 5. Ellul MA, Benjamin L, Singh B, Lant S, Michael BD, Easton A, et al. Neurological associations of COVID-19. Lancet Neurol. 2020;19: 767–783.
6. 6. Jordan RE, Adab P, Cheng KK. Covid-19: risk factors for severe disease and death. BMJ . 2020. p. m1198.
7. 7. Lima M, Siokas V, Aloizou A-M, Liampas I, Mentis A-FA, Tsouris Z, et al. Unraveling the Possible Routes of SARS-COV-2 Invasion into the Central Nervous System. Curr Treat Options Neurol. 2020;22: 37.
8. 8. Rothan HA, Byrareddy SN. The epidemiology and pathogenesis of coronavirus disease (COVID-19) outbreak. J Autoimmun. 2020;109: 102433.

9. 9. Netland J, Meyerholz DK, Moore S, Cassell M, Perlman S. Severe acute respiratory syndrome coronavirus infection causes neuronal death in the absence of encephalitis in mice transgenic for human ACE2. J Virol. 2008;82: 7264–7275.
10. 10. Varatharaj A, Thomas N, Ellul MA, Davies NWS, Pollak TA, Tenorio EL, et al. Neurological and neuropsychiatric complications of COVID-19 in 153 patients: a UK-wide surveillance study. Lancet Psychiatry. 2020;7: 875–882.
11. 11. Huo L, Xu K-L, Wang H. Clinical features of SARS-CoV-2-associated encephalitis and meningitis amid COVID-19 pandemic. World J Clin Cases. 2021;9: 1058–1078.
12. 12. Radmanesh A, Raz E, Zan E, Derman A, Kaminetzky M. Brain Imaging Use and Findings in COVID-19: A Single Academic Center Experience in the Epicenter of Disease in the United States. AJNR Am J Neuroradiol. 2020;41: 1179–1183.
13. 13. Garg RK, Paliwal VK, Gupta A. Encephalopathy in patients with COVID-19: A review. J Med Virol. 2021;93: 206–222.