A Comprehensive Overview of the Newly Emerged COVID-19 Pandemic: Features,

SARS-CoV-2 adopts a dodgy mechanism to escape the host’s innate immune response and successfully infect healthy individuals. Since SARS-CoV-2 and SARS-CoV show close clinical manifestations, SARS-CoV-2 has unique pathogenesis and biochemical processes comparable to SARS CoV [121]. Following SARS-CoV infections, the release of IFN-stimulated genes (ISGs) induced by the type I interferon (IFN) occurs against the viral replication process. In response to this defense activity by host cells, SARS-CoV-2 secretes a minimum of eight antagonizing factors that neutralize the ISG’s activity [122]. However, the immune response mediated by the host’s defense system poses a critical role in limiting viral dissemination. Nevertheless, excess promptness of the immune cells, coupled with lytic stress by viral invasion, results in severe disease outcomes. The most common symptoms manifested at the early stage include patients with acute body pain, pneumonia, dry cough, and fever [121,123]. Further progress rapidly results in acute respiratory stress syndrome (ARDS), septic shock, and organ failure, followed by death [123]. After COVID-19 infection, the development of ARDS and the subsequent damages occurring at the alveolar type II pulmonary cells as well as in the ciliated epithelium cells of the airways suggest that ACE2 is abundant in lung cells, acting as a gateway for virus entry [124]. A similar mode of the inflammatory cascade has been reported in both SARS-CoV-2 and SARS-CoV infected patients. A bulk load of pro-inflammatory cytokines (e.g., interleukin (IFN-γ, IFN-γ-induced protein 10 (IP10), IL-1, IL-6, IL-12)), monocyte chemoattractant protein-1 (MCP1), and macrophage inflammatory proteins1A (MIP1A) were found in serum collected from previously infected patients with SARS-CoV. These immune cells are also related to severe lung damage and pulmonary inflammation [125]. In addition, a high level of pro-inflammatory cytokines such as TNF-α, IL1β, IL-2, IL7, and MCP1were found in samples of SARS-CoV-2 infected patients. On the other hand, (ICU) intensive care unit patients of COVID-19 contained a greater load of cytokines such as TNF-α, GSCF, MCP1, and IP10 compared to the non-ICU patients. This suggests that cytokine storms can be the underlying cause of severe disease manifestation [31]. The study reports that a high cytokine concentration has a reversible correlation with the total immune cell (T, CD4+, and CD8+) counts in SARS-CoV-2 infection. Hence, lower T cell counts can be a potential biomarker for risk stratification of patients infected with COVID-19 [126]. Besides, other findings reported that adults (males) are more vulnerable to SARS-CoV-2 infection than young children [121,123]. A similar finding was observed in the experiment on a primate model called Cynomolgus macaque (crab-eating monkey) [127]. Further follow-up studies are warranted from the scientific community to get a better understanding of the virulence factors of SARS-CoV-2 [128].