Introduction
In December 2019, a sudden outbreak of an acute respiratory syndrome caused by a novel coronavirus was reported for the first time in Wuhan, Hubei Province, China. The World Health Organization (WHO) named the disease as COVID-19 and three months later, declared it a global pandemic. This virus is highly contagious and affects the lower and upper respiratory system. Evidence shows that coagulation disorder is often seen in COVID-19 patients and its occurrence is higher in severe cases [1, 2]. Due to the insufficient information about coagulopathy of COVID-19, in this narrative review study, we aims to investigate the genetic structure, pathogenesis, clinical manifestations of COVID-19 and the relationship of this disease with blood coagulation disorders in patients with COVID-19.
Materials and Methods
This is a narrative review study. Articles were searched using the keywords COVID-19, Respiratory infection and Coagulopathy in Google Scholar, PubMed, Google Springer and Science Direct databases.
Results
The novel coronavirus belongs to the subfamily Coronavirinae and the family Coronaviridae. This virus is one of the enveloped viruses that have a diameter of 80-120 nm and has four variants: Alpha, beta, delta and gamma [3]. It uses angiotensin-converting enzyme 2 (ACE2) as a receptor and infects cells with ACE2 through the receptor-binding domain found in the Spike (S) protein. Most common clinical symptoms of COVID-19 include: Fever, cough, fatigue, diarrhea, and vomiting, which are similar to other coronaviruses with animal origin [8, 10]. Acute respiratory distress syndrome occurs about 9 days after the infection. In addition to the lungs, this virus involves heart, kidney, liver, eyes, and the nervous system. Infection caused by COVID-19 activates systemic inflammatory responses as a part of the innate immune response [13]. The activation of the host’s defense system leads to the activation of hemostatic factors and finally causes the generation of thrombin, which is known as inflammation of thrombosis or immunothrombosis. The receptor for virus adhesion on endothelial cells is ACE2; therefore, when the virus enters the vascular endothelial cell, it causes viral replication, infiltration of inflammatory cells, endothelial cell apoptosis, and capillary prothrombotic effects [20]. Recent studies have shown the occurrence of venous and arterial thrombosis, including deep venous thrombosis, pulmonary embolism, ischemic stroke, and myocardial infection in patients with COVID-19 admitted to the intensive care units [22, 23]. Virchow’s triad, which includes blood flow stasis, vascular wall damage, and hypercoagulability, can also be a mechanism in COVID-19. Hospitalized patients with confirmed or suspected COVID-19 should have coagulation tests at the time of admission, including D-dimer, prothrombin time test, activated partial thromboplastin time test, fibrinogen test, and platelet count, since these tests provide a useful prognosis [32].
Discussion
The symptoms and prognosis of COVID-19 depend on many factors, such as patient’s age, underlying diseases, the type of virus, etc. One of the important features in infected patients is the hemostatic disorders that are associated with changes in indicators such as platelet count, fibrinogen/fibrin degradation products, D-Dimer, and fibrinogen. Therefore, according to changes in the hemostatic system of patients with COVID-19, anticoagulant treatments are recommended along with supportive treatments for these patients.

Ethical Considerations
Compliance with ethical guidelines
Ethical principles in writing this article were observed in accordance with the guidelines of the National Ethics Committee and the Committee on Publication Ethics (COPE).

Funding
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for profit sectors.

Authors' contributions
All authors met the writing standards based on the recommendations of the International Committee of Medical Journal Editors (ICMJE).

Conflicts of interest
The authors declare no conflict of interest.

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