COVID-19 جهش یافته
Abstract
Introduction
Prevalence and epidemiology
Virus structure
Clinical manifestation and symptoms
Preventions
Diagnosis
Treatment
Conclusions
Transparency declaration
Acknowledgement
References
Abstract
Coronavirus disease 2019 SARS-CoV-2 (COVID-19) is a zoonotic virus causing a variety of severe respiratory diseases. SARS-CoV-2 is closest to SARS-CoV and MERS-CoV in structure. The high prevalence of COVID-19 is a result of a lack of symptoms at onset. Our study aimed to present an overview of the virus in terms of structure, epidemiology, symptoms, treatment and prevention. Whole genome sequences and some viral proteins were investigated to determine gaps and changes in alternation of nucleotides and amino acid sequences. We evaluate 11 complete genome sequences of different coronaviruses using BAST and MAFFT software. We also selected seven types of structural proteins. We conclude that COVID-19 might produce new mutations, specifically in glycoproteins, so caution and complete preparation by health authorities is required.
Introduction
Novel coronavirus disease 19 (COVID-19) first emerged on 31 December 2019 in Wuhan city, China. COVID-19 is classified as the seventh member of the subfamily Orthocoronavirinae under the family Coronaviridae. Most members of this family are zoonotic viruses transmitted to humans through contact with infected animals. Although bats and snakes are the natural reservoir of most coronaviruses, there is no evidence so far that COVID-19 originated in or was transmitted from a seafood market [1]. Comparison of the lipid rafts of coronaviruses has indicated that the new strain COVID-19 has 80% identity with severe acute respiratory syndrome coronavirus (SARS-CoV). Lipid molecules such as caveolins, clathrins and dynamin have a fundamental role in the internalization of viruses. These molecules are involved in the entry of viruses into host cells, and targeting host lipids is being studied as an antiviral strategy and could have various applications [2]. COVID-19 seems to need to bind to the angiotensin-converting enzyme-2 receptor on the membrane host cell to enable it to infect the host cell upon coupled with a reliance of serine protease TMPRSS2. This intracellular protein seems to be a determinant of the virus ability to infect the cell [3].