Journals / İzmir Tepecik Eğitim Hastanesi Dergisi / 2020 / Cilt: 30 - Sayı: 0

Overview of COVID-19 Infection from Immunological Perspective

İmmünolojik Açıdan COVID-19 Enfeksiyonuna Bakış

Pages
101–111
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

In ACE, it is estimated that cellular uptake can be promoted by binding of virus peptides bound to immune complexes to FcγRIIa on the cell surface.

📌 3 Key Takeaways

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Objective & Hypothesis:Coronaviruses are enveloped, positive, single-stranded RNA viruses with ~ 30 kb genetic material.
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Key Findings & Data:Defined as a functional receptor for the spike protein of SARS-CoV-2, ACE2 is highly expressed in lung epithelial cells.
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Conclusion & Impact:In ACE, it is estimated that cellular uptake can be promoted by binding of virus peptides bound to immune complexes to FcγRIIa on the cell surface.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Coronaviruses are enveloped, positive, single-stranded RNA viruses with ~ 30 kb genetic material. The life cycle of the virus in the host takes place in five steps: attachment, penetration, biosynthesis, maturation and release. Defined as a functional receptor for the spike protein of SARS-CoV-2, ACE2 is highly expressed in lung epithelial cells. Therefore, it primarily affects the respiratory system and also has effects on other organ systems. Understanding the antigen presentation of the SARS-CoV-2 will help us understand the pathogenesis of COVID-19 infection. Here, it is thought that the diversity of human leukocyte antigens (HLA) may be important in contracting the disease, and response to the immune system. HLA-DR * 0301, HLA-Cw * 1502 and HLA-A * 0201 alleles have been reported to be associated with protection from SARS infection. The manifestations, which start with the increase in tne number of proinflammatory cytokines in some patients, induce a dysfunctional immune response that triggers a cytokin storm mediating widespread lung inflammation by activation in other inflammatory cytokines. Antibody dependent increase (ADE) is another controversial mechanism in the pathogenesis of COVID-19 infection, and it has been reported to cause increased viral infection damage. In ACE, it is estimated that cellular uptake can be promoted by binding of virus peptides bound to immune complexes to FcγRIIa on the cell surface.

Özet

Koronavirüsler, ~ 30 kb’lık genetik materyale sahip, zarflı, pozitif, tek sarmallı RNA virüsleridir. Virüsün konakçıdaki yaşam döngüsü, bağlanma, penetrasyon, biyosentez, olgunlaşma ve salıverme olmak üzere beş adımda gerçekleşir. SARS-CoV-2’nin spike proteini için fonksiyonel bir reseptör olarak tanımlan ACE2, akciğer epitel hücrelerinde yüksek oranda belirtilmektedir. Bu nedenle öncelikli olarak solunum sistemini etkiler ve diğer organ sistemleri üzerine de etkileri olur. SARS-CoV-2’nin antijen sunumunun anlaşılması, COVID-19 patogenezini anlamamıza yardımcı olacaktır. Burada insan lökosit antijenlerinin (HLA) çeşitliliğinin hastalığa yakalanma ve bağışıklık sisteminin yanıtında önemli olabileceği düşünülmektedir. HLA-DR*0301, HLA-Cw*1502 ve HLA-A*0201 alellerinin SARS enfeksiyonundan korunma ile ilişkili olduğu bildirilmiştir. Bazı hastalarda proenflamatuar sitokinlerin artışıyla başlayan tablo diğer enflamatuvar sitokinlerinde devreye girmesiyle yaygın akciğer iltihabına aracılık eden bir sitokin fırtınasını tetikleyen işlevsiz bir bağışıklık tepkisi ortaya çıkartır. Antikora bağımlı artış (ADE) COVİD-19 patogenezinde tartışılan bir diğer mekanizmadır ve viral enfeksiyon hasarının artışına neden olabileceği bildirilmiştir. ADE de bağışıklık komplekslerine bağlanan virüs peptitlerin hücre yüzeyinde FcγRIIa’ya bağlanmaları yoluyla hücresel alımını teşvik edilebileceği tahmin edilmektedir.

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Cite This Article

SOYÖZ, M., AYNA, T. K., PİRİM, İ. (2020). Overview of COVID-19 Infection from Immunological Perspective. İzmir Tepecik Eğitim Hastanesi Dergisi, Cilt: 30 - Sayı: 0, 101–111. https://ajindex.com/articles/168539

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