Koronavirüs (COVİD-19) ve Sinir Sistemi; Bilinenlerin Ötesinde

Year 2020, Volume: 1 Issue: 2, 58 - 66, 01.06.2020

Ayşegül Yurt Mustafa Saygın

Abstract

Son yirmi yılda farklı formlarda karşımıza çıkan korona virüsler, hafif soğuk algınlığından şiddetli vakalara neden olabilen bir virüs ailesidir. Son olarak 2019 yılının sonlarında ortaya çıkan yeni tip korona virüs (Covid-19, 2019-nCoV, SARS-CoV2) oldukça bulaşıcı özelliğe sahiptir. Mortalite oranı düşük, morbidite oranı ise yüksektir. Bu güne kadar yaklaşık 17 milyon vakanın görülmesine ve 700 bin kadar ise ölüme neden olmuştur. Korona virüsler tek sarmallı RNA genomuna sahip zarflı virüslerdir. Genetik ve antijenik özelliklerine dayanarak dört alt gruba ayrılır. Alfa-coronavirüsler, Beta-coronavirüsler, Delta-coronavirüsler ve Gama-coronavirüsler. SARS-CoV2’nin hedef reseptörü ACE2 enzimidir. ACE2 enzimi; vücutta yaygın olarak akciğerler, kardiyovasküler sistem, böbrekler, sinir sistemi ve kılcal damar endoteli dahil birçok dokuda eksprese edilir. Dolayısı ile kan dolaşımına bir kere vücuda giren virüs birçok dokuda semptomlara neden olur. Koronavirüsler; solunum, sindirim, hepatik ve nörolojik hastalıklara neden olur. Nöroinvazif eğilim gösteren korona virüsler; kan beyin bariyerinin kılcal damar endotelinde yıkıma neden olur, sitokin fırtınası ile damar geçirgenliğini artırarak veya periferik sinirlerde ki (koku siniri, vagus siniri) ACE2 enzimine tutunarak santral sinir sistemine ulaşabilir. Nörodejeneatif hastalıkları arttırabilir, presemptomatik hastaları semptomatik hale getirebilir. Nörodejeneratif hastalıkların altta yatan mekanizmasının sitokin fırtınası olması, Covid-19’lu hastaların daha sonra ki süreçlerde de nörodejeneratif hastalık profili açısından değerlendirilmesi gerektiği öngörülmektedir. Bu çalışmanın amacı SARS-CoV2’nin sinir sistemi üzerinde ki olası etkilerine ve enfekte olan bireyleri daha sonraki süreçte olası nörodejeneratif hastalıklar açısından değerlendirilmesine dikkat çekmektir.

Keywords

SARS-CoV2, Sinir Sistemi, ACE2 enzimi, Sitokin Fırtınası, Uyku

Coronavirus (COVID-19) and Nervous System; Beyond the Known

Abstract

Corona viruses, which have appeared in different forms in the last two decades, are a family of viruses that can cause severe cases from mild colds. Finally the new type of corona virus (Covid-19, 2019-nCoV, SARS-CoV2), which appeared in late 2019, has a highly contagious feature. The mortality rate is low and the morbidity rate is high. Until today about 17 million cases and it caused the death of approximately 700 thousand patients. Corona viruses are enveloped viruses with a single stranded RNA genome. It is divided into four subgroups according to its genetic and antigenic properties. Alpha-coronaviruses, Beta-coronaviruses, Delta-coronaviruses and Gamma-coronaviruses. The target receptor of SARS-CoV2 is the ACE2 enzyme. ACE2 enzyme is commonly expressed in the body in many tissues, including the lungs, cardiovascular system, kidneys, nervous system, and capillary endothelium. Therefore, the virus that enters the blood circulation once causes symptoms in many tissues. Coronaviruses; causes respiratory, digestive, hepatic and neurological diseases. Corona viruses with neuroinvasive tendency; it causes destruction in the capillary endothelium of the blood brain barrier, it can reach the central nervous system by increasing the vascular permeability by storming cytokines or by attaching to the ACE2 enzyme in the peripheral nerves (smell nerve, vagus nerve). It can increase neurodegenerative diseases and make presymptomatic patients symptomatic. It is to predict that the underlying mechanism of neurodegenerative diseases is cytokin storm, and patients with Covid-19 should be evaluated in terms of neurodegenerative disease profile later on. The aim of this study is to draw attention to the possible effects of SARS-CoV2 on the nervous system and the evaluation of infected individuals in terms of possible neurodegenerative diseases in the later process.

Keywords

SARS-CoV2, Nervous System, ACE2 Enzyme, Cytokine Storm, Sleep

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