Morphological changes in host airway epithelium following SARS-CoV-2 infection: A pathophysiological perspective

COVID-19 continues to affect the world since its emergence, with new strains evolving during repeated summer and winter waves. The SARS-CoV-2 variants of concern (VOCs) show increased infective potential for the host due to mutations in their spike protein (S), which strengthens the binding between the target receptor of the spike protein, i.e., the angiotensinconverting enzyme (ACE2), located on airway epithelial cells as well as other parts of the body like intestinal epithelial cells, thus allowing the virus to cause much more profound infection in the host cells. This review focuses on the progression of morphological changes in airway epithelial cells after exposure to SARS-CoV-2. The extent of damage or resilience in these cells is crucial in determining the degree of pathogenesis the virus can exert in the host body over time. We also examine recent cellular and animal models utilized to investigate the pathophysiology of SARS-CoV-2, which may provide new insights into its biology.