Due to the accumulation of un-cleaved angiotensin II, the activated inflammatory cells lead to excessive cytokine synthesis and release (cytokine storm). from SARS-CoV-2 or severe acute respiratory syndrome coronavirus 2, triggered nationwide shutdown in most nations around the world. Consequently, the world is facing a huge socioeconomic disaster and irreversible financial problem. In China, novel ?CoV or SARS-CoV-2 was initially found in adults suffering from acute lower respiratory tract infection (LRTI) of uncertain origin. (Chan et al., 2020) As no age group is immune to the new virus, patients aged 60 or above and those with co-morbidities showed extreme symptoms. Most people affected by the COVID-19 are either asymptomatic or have a mild type of virus strains. It is a highly infectious disease that is primarily transmitted through respiratory droplets and near contact with infected persons or polluted items. It also increases the risk of nosocomial infections. (Cascellaet al., 2020; WHO, 2020) The COVID-19 has a significantly low mortality rate but a much higher rate of infection compared to SARS disease. (Ruan et al., 2019; Mahase, 2020) While the COVID-19 infection is widely spread through respiratory droplets, it is possible to take a fecal-oral route. Apart from sputum and pharyngeal swabs, the virus was detected in feces. (DAmico et al., 2020) A positive COVID-19 nasopharyngeal swab had identified and verified the vertical transmission of SARS-CoV-2. The new virus has a median incubation time of 5.2 days and the majority of patients develop the disease within 11.5 to 15.5 days. Therefore, people who have been exposed to infection are advised to be in quarantine for 2 weeks. (Li et al., 2020) 2.?Covid-19 immunological mechanisms SARS CoV-2 resembles SARS CoV; it has densely glycosylated spike (S) proteins S1 fraction with receptor-binding domain (RBD) attaching to the angiotensin-converting enzyme 2 receptor (ACE-2 R) with 10C20x greater affinity compared to SARS CoV. (Wrapp et al., 2020) This receptor is primarily found in both types of human alveolar FTI-277 HCl epithelial cells (type II type I). (Zhou et al., 2020, Tian et al., 2020, Gui et al., 2017) It is expressed by endothelial cells along with gastrointestinal (esophageal and intestinal), epithelium, and cardiac myocytes. (Meng et al., 2020; Xiong et al., 2020) After binding UVO to ACE-2 R, the virus employs its unique polybasic S1/S2 protease cleavage site by inserting SPRR in the spike protein. Transmembrane protease serine (TMPRSS) displayed on host cells detects and cleaves the site for fusion protein (S2 fraction) exposure, enabling the viral membrane to fuse with that of the host cell. (Meng et al., 2020) ACE-2 R, as well as TMPRSSs has also shown to be significantly co-expressed in absorptive enterocytes, upper esophageal epithelium, and alveolar type 2 pneumocytes. It implies that the new virus can FTI-277 HCl enter the host through the alveolar epithelium FTI-277 HCl along with the esophageal and intestinal epithelium. Therefore, the possible target tissue of the new virus could co-express ACE-2 R and TMPRSS. (Meng et al., 2020) This membrane fusion allows viral RNA to be internalized into the host cells cytoplasm, where it replicates and translates FTI-277 HCl to form new viral proteins. Viral aggregation is the last?stage?before liberating virions from infected cells. It comprises nucleocapsid (N) proteins that bind to RNA molecules. The viral aggregations are protected by membrane and envelop protein; consequently, virions with an ability to infect the surrounding cells are developed. SARS CoV-2 infection primarily impairs type II pneumocytes (play an important.