1 Introduction In December 2019, a severe pneumonia outbreak by Severe Acute Respiratory Syndrome associated coronavirus (SARS-CoV-2) had supervened in Hubei province, Wuhan, China [1,2]. Among the viruses that belong to Coronaviridae family and pathogenic to human beings, the SARS-CoV-2 has been identified as the third virus after SARS-CoV and Middle East Respiratory Syndrome associated coronavirus (MERS-CoV) to create a pandemic situation [3]. The SARS-CoV-2 belongs to the family Coronaviridae. Genealogical examination of the SARS-CoV-2 revealed that it belongs to the genera beta coronavirus and exhibited 96% homology sequence similarity with Bat SL-CoV; whereas, the bat is an intermediate host or not needs to be elucidated [2]. The diameter of SARS-CoV-2 ranges between 50 and 200 nm [4]. This virus possesses four distinct proteins that provide the virus its structure. The outermost layer consists of glycoprotein spikes followed by an envelope, a membrane, and a nucleocapsid layer towards the inner side. The nucleocapsid layer holds the viral genome, RNA. The nucleocapsid layer, envelope, and the spike membrane provide a protective layer for the viral genome [5]. The RNA of CoVs is a single-stranded positive-sense RNA (+ssRNA), which is ~30 kb possessing 5′-cap and 3′-poly-A tail [6]. After entering the host cell, the SARS-CoV-2 undergoes replication by using the host's machinery and synthesizes N, M, E, and S structural proteins. The negative strand of the RNA genome is produced using a positive-strand as a template. At the time of the process of replication in the host cell, the M protein attaches to the membranes of the endoplasmic reticulum, and the N protein binds to the genome. Nsp proteins help the RNA to assemble into a helical structure which enters the lumen of the endoplasmic reticulum. The viral progenies produced undergo exocytosis and enter the extracellular space [7]. Dr. TedrosAdhanom Ghebreyesus, Director-General of world health organization (WHO) on February 11, 2020, has declared the name of the pandemic condition as coronavirus disease-19 abbreviated as COVID-19. The symptoms of COVID-19 include infection to the lower respiratory tract, pneumonia ranging from mild to severe, dry cough, lymphopenia, fever, and fatigue [6,8]. Upon mild infection, the patients present dry cough, vomiting, diarrhea, fatigue, and fever as symptoms whereas in case of severe infection, one week later the disease onset the condition of the patient may worsen resulting in hypoxemia, septic shock, acute respiratory distress syndrome (ARDS), metabolic diseases and may also lead to death in some cases [9]. Apart from the epidemic condition created by the coronavirus, it has been found that the affected individuals, along with other comorbidities such as cardiovascular diseases, type 1 and type II diabetes, and renal diseases, are found to be severely ill compared to the individuals infected only by the coronavirus. The controversy has been raised when Lei Fang, a postdoctoral researcher, and his colleagues suggested that “Patients with cardiac diseases, hypertension or diabetes who are treated with ACE2-increasing drugs are at higher risk for severe COVID-19 infection and, therefore, should be monitored for ACE2-modulating medications, such as angiotensin-converting enzyme inhibitors (ACEi) or angiotensin receptor blockers” [10]. In response to the above statement, the European Society of Cardiology on March 13 and the American College of Cardiology, the American Heart Association, and the Heart Failure Society of America endowed a common statement on March 17 which mentioned that “since there is no scientific evidence behind ceasing the usage of ACEi and angiotensin type II receptor blockers (ARBs) for the patients affected by COVID-19 possessing other comorbidities such as high blood pressure, diabetes mellitus, cardiovascular problems and renal diseases” [11]. The pandemic condition caused by SARS-CoV-2 has brought a whole world to lockdown. To safeguard the human, from the deadly virus, a lot of research has been carried out.