Genomic Variation and Treatment Strategies of COVID-19: A Descriptive Review

Coronavirus disease 2019 (COVID-19) was spread across China and affected more than 180 countries worldwide to date. SARS-CoV-2 is a beta coronavirus that shows genomic similarity with bat coronaviruses. The intermediate source in human viral transmission is caused by dromedary camels for MERS-CoV and civet cats for SARS-CoV. Transmission of the virus from human-to-human is achieved through close contact with infected persons. The genome of the coronavirus consists of four structural proteins, including Spike (S), Membrane (M), Envelop (E), and Nucleocapsid (N) proteins. These structural proteins are encoded within the genome 3' end. The spike protein is responsible for virus attachment to the host cell surface receptors (angiotensin converting enzyme-2 receptor), resulting in fusion and subsequently cell damage. The N protein, after binding, causes RNA genomic changes. The accessory proteins present in SARS-CoV open read frames (ORFs) are very similar to COVID 19. The COVID-19 infection triggered a number of deaths and even now affecting a number of confirmed cases. Coronavirus patients are characterized by pneumonia, cytokine storms, weakened lymphocytes, lymphocytopenia, and respiratory failure. However, the lack of antiviral vaccines permits emergency clinical trials since January 2020. Recently, several anti-viral drugs are being repositioned and restructured as part of an immediate investigation. In this review, we discussed the genomic sequence of SARS-CoV-2, its different features and current therapeutic strategies to combat this serious condition.