fig8

Figure 8. The diagram illustrates the different stages of SARS-CoV-2 infection and potential treatment strategies to target specific steps. (A) SARS-CoV-2 is activated by TMPRSS2, which allows it to attach to the glycosylated ACE2 receptor found on alveolar epithelial cells. The fusion of the viral capsid with the host cell membrane results in endocytosis. (B) Under optimal acidic conditions in the endosome and lysosome, ss(+) viral RNA is generated through fusion. (C) The RNA is then transcribed and translated to synthesise polyproteins which undergo further maturation through cleavage by HIV proteases, resulting in non-structural proteins. (D) The non-structural proteins combine within double-membrane vesicles (DMVs) to form the replication-transcription complex (RTC). The RTC increases the number of RNA copies and generates essential proteins. Assembling the necessary components leads to the formation of the complete viral particle. The release of the complete virion particle is associated with increased cytokine levels and acute lung injury. The figure also highlights possible treatment inhibitors for each step, such as monoclonal antibodies (mAb) targeting specific viral proteins, ACE2 inhibitors (ACE2i), TMPRSS2 inhibitors, Cathepsin B/L inhibitors, ACE inhibitors (ACEi), angiotensin receptor blockers (ARBs), and Janus-Associated Kinase inhibitors (JAKi).