Pathophysiology

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causal pathogen of the novel coronavirus disease 2019. This novel Covid-19 has created a serious public health crisis throughout the world. The primary symptoms of coronavirus infection are common cold and influenza-like illness and with time it causes pneumonia. Although various studies are going on throughout the world, its actual pathophysiology is not very well clear to date. The Coronavirus is a positively charged single-stranded RNA virus. This virus gets easily transmitted from human to human. Numerous investigations have been found that the virus enters into the human body via its spike (S) proteins. The S-protein binds to ACE2 receptors and silently comes in contact with alveoli via blood. This entry hypersensitizes various receptors, epithelial cells, macrophages, T-cells, dendritic cells and thus implants proinflammatory cytokines and chemokines, resulting in stressful conditions. Studies found that Hemagglutinin-Esterase protein, Spike protein, Nucleocapsid protein, small envelope protein, internal proteins, group-specific proteins take part in viral pathogenesis, whereas, replication proteins (eIF4A, Cyclophilin, 3CLpro, RdRp) participates in Coronaviruses (CoVs) replication and translation phases, influencing both pathogenesis and pathophysiological conditions. In this chapter, we elaborate on viral pathogenesis, the various functions of proteins, structural, enzymatic, and accessory that are linked with the pathological conditions and will also highlight the correlation causing physiological alteration associated with this infection.

Keywords: ACE2 receptors, Covid-19, Hemagglutinin-Esterase protein, Life cycle, Membrane protein, Nsp1 protein, Nsp3 protein, Nsp8 primase, Nsp12 polymerase, Nsp13 helicase, Nsp14 protein, Nsp15 protein, Nsp16 protein, Nucleocapsid protein, Orf3b, Orf6, Orf7a, Pathogenesis, Pathophysiology, Spike proteins, Thrombosis, Transmission.