Abstract

The article presents literature data numerous studies of patients with COVID-19. The available information helps to explain the nature and structure of the virus, the ways of penetration and its distribution in the human body, its interaction with the immune, nervous, endocrine, vascular, muscular systems, as well as the pathogenesis, clinic, diagnosis and treatment of this contingent of patients. Due to tropisms SARS-CoV-2 to the human cells specifi c S glycoprotein this virus can bind receptor human angiotensin-converting enzyme 2 (ACE-2), fuse with host cells and disseminate in the organism. Renin-angiotensin-aldosteron system (RAAS) plays an important role in regulation of blood vessels, heart, kidneys functions. ACE-2 has an infl uence on the infl ammatory, fi brotic and immunomodulatory mechanisms. Inhibition of these protection functions due to spread SARS-CoV-2 in human body leads to the progression of cardiovascular, renal and pulmonary diseases. Some authors describe indirectly the viral entry into the brain parenchyma by infecting the T-lymphocytes, that usually is accompanied by infl ammatory reactions with an increase in the specifi c cytokines such as interleukins (IL) — 6, IL-8, tumor necrosis factor, monocyte chemoattractant protein-1 (MCP-1). The peculiarities of the binding of the virus to the human cells are the presence of neurotropic properties and the ability to change the permeability of blood brain barier (BBB). Other authors note that the virus crosses the BBB directly through the olfactory neurons and also the brain’s circumventricular organs structures, surrounding the third and fourth ventricles, and promote the infection of nervous system. It can also cause intravascular coagulation and blood clotting, which may lead to various diseases of the nervous system. In this regard, an important task for neurologists is to further study the eff ect of the COVID-19 virus on the nervous system and prevent the occurrence of its complications.

Highlights

  • It had been one year and a few months that the world had been struggling with the emergent SARS-CoV-2 infection, which had spread with a very strong agility to reach almost every corner of the globe in just few months

  • Evaluation of immune response childrens with CNS encephalitis-like infection and respiratory tract infection due to COVID-19 indicate on significantly higher level of cytokines such as granulocyte macrophage colonystimulating factor (GM-cerebrospinal fluid (CSF)), IL-6, IL-8, monocyte chemoattractant protein-1 (MCP-1), and GM-CSF in their CSF compared to serum samples

  • As well as symptoms lesion of respiratory system and gastrointestinal tract (GIT) we meet with COVID-19-associated acute cerebrovascular system (CVS) diseases such as ischemic and hemorrhagic stroke, thrombosis of cerebral venous sinuses, inflammatory coagulopathy

Read more

Summary

Introduction

It had been one year and a few months that the world had been struggling with the emergent SARS-CoV-2 infection, which had spread with a very strong agility to reach almost every corner of the globe in just few months. ACE-2 mechanism of action was seen in models of diseases like obesity, cerebral ischemia, atherosclerosis, and others by causing the reduction in cytokine production and interfering with fibrotic signaling pathways [11] This can exacerbate inflammatory symptoms in SARS-CoV-2 infected patients. In articles [23,24] describe the clinical case of minor stroke SARS-Cov-2 positive patient with comorbid pathology as hypertension, type 2 diabetes, chronic renal disease, dyslipidemia and ischemic heart disease with a myocardial infarction Most of the imaging outcomes of the FDG-PETscan around the 19th-23rd days of the viral infections show bilateral prefrontal and left-sided parieto-temporal hypometabolism and a slight hypermetabolism within the cerebellar vermis [23] This clinical finding on the FDGPET-scan is a confluent finding consistent with most of COVID-19 patients displaying cognitive impairments. Addiitional assignment of tocilizumab, monoclonal antibody, to dexamethasone therapy usually use to get better survival of the patients with quick respiratory decompensation [38,39]

Conclusion
Меркулова Ольга Юріївна
Меркулова Ольга Юрьевна
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call