Extended Abstract
Introduction
In late December 2019, a case of pneumonia with unknown etiology was reported in Wuhan, Hubei Province, China, whose clinical features were very similar to those of viral pneumonia. The World Health Organization named this virus as “COVID-19” [1, 2]. In this review article, we discuss the genetic structure, pathogenic mechanism, clinical manifestations, diagnosis, treatment, and prevention of COVID-19.
Materials and Methods
The present study is a systematic review. The articles were searched using the keywords: COVID-19, coronavirus, and respiratory infection.
Results
Coronaviruses are positive-sense RNA viruses. Among them, the homology and pathogenesis mechanism of SARS-CoV is very similar to those of COVID-19 [3، 4]. COVID-19 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. In acidic pH, lysosomes and endosomes are broken down by catalytic enzymes into two subunits, S1 and S2. In cell cytoplasm, the virus begins to replicate with the help of its RNA polymerase, and new viruses infect other cells [5-9]. COVID-19 is also associated with demographic status. The highest mortality rate is related to the elderly men with a mean age of 75 years with a history of underlying disease. The cellular immunity, which is the most important part of the immune system in protecting against viral infections, is weakened in the elderly people due to COVID-19. The mortality rate for this virus is 3.4% [1, 12, 13]. Bats are considered the natural host of this virus. Direct contact and respiratory droplets are the most common ways that the virus spreads in the community [2, 15]. 
The most common clinical signs of COVID-19 infection are fever, cough, and fatigue. In addition to the lung damage, the virus causes damage in other tissues [18]. The neurological symptoms of the virus are related to lack of oxygen in the blood and inflammation of the brain. Inflammation of the brain can be caused indirectly by a cytokine storm (autoimmune encephalitis) or directly by bypassing the blood-brain barrier (viral encephalitis) [19, 20]. COVID-19 causes neurovascular complications by causing venous and arterial thrombosis [21].
The combined use of CT imaging, clinical signs, and laboratory tests can help with the initial diagnosis of COVID-19 pneumonia. Lymphopenia, thrombocytopenia, and elevated CRP and D-dimer levels are observed. High levels of IL-6 and IL-10, as well as low levels of CD4 + T and CD8 + T cells are associated with disease severity [23-26]. In this disease, the window period lasts about 7 days and is when the antibody is not yet produced. IgM, as the first antibody, begins to synthesize on the 7th day and deactivated on day 21 of the disease. IgG starts synthesizing on the 14th day and continues to be produced. The asymptomatic period of the disease is from the time of infection to the 5th day, and the period of onset of clinical symptoms is from the 5th to the 8th day. The disease begins to subside on the 14th day, which coincides with the onset of humoral immune response shift from IgM to IgG. The disease disappears by day 28 [27, 28].
Detection of nucleic acid acids is a standard method for determining coronavirus infection, although these methods have high specificity but low sensitivity with false negative rate, and are time-consuming [1]. Common treatments, including hydroxychloroquine are often symptomatic, although Remdesivir has recently been introduced as an antiviral drug for this purpose [9, 30]. Hydroxychloroquine, by accumulating in intracellular organs such as endosomes and lysosomes, increases their pH. It increases the pH to prevent endocytosis of the virus and its entry into the cytoplasm. With its immunomodulatory effect, this drug also prevents cytokine storms [7, 30, 31].
Some studies have suggested that the cause of death by COVID-19 infection is the activity of mycobacteria such as tuberculosis and Mycobacterium avium and the resulting pneumonia. For this reason, tuberculosis infection, whether active or latent, increases the severity and progression of the COVID-19. Therefore, patients who received the Bacillus Calmette–Guérin (BCG) vaccine before the disease are more resistant to COVID-19. The BCG vaccine stimulates the immune system response to a large number of antigens effective in incidence of infectious diseases. One of the involved mechanisms is the activation of heterologous lymphocytes, including Natural Killer (NK) and Natural Killer T (NKT) memory cells. The BCG vaccine also increases IL-1β production against viral infections by applying epigenetic changes [37-40].
Discussion
COVID-19 is a serious and dangerous infectious disease whose symptoms are similar to SARS including fever, cough and fatigue. The disease is mostly transmitted through respiratory droplets and close contact. It is a major threat to the health and safety of the world and must be prevented from spreading. Since the exact mechanism of the disease by the virus is unknown and no specific drug or vaccine has been introduced for it, the most important thing to do now is to stop the transmission cycle [1، 9].
Ethical Considerations
Compliance with ethical guidelines
Ethical principles in writing this article have been 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.