Journal: Current Microbiology

Article Title: Molecular Insights into the Crosstalk Between Immune Inflammation Nexus and SARS-CoV-2 Virus

doi: 10.1007/s00284-021-02657-9

Figure Lengend Snippet: Dysregulated complement cascade in SARS-COV-2 infection: SARS-COV-2 has been found to directly activate MASP2 and induce LP via N proteins. While S proteins activates the CP, AP is also stimulated in the advanced stages. Sequential aberrant activation of C3 compliment fraction promotes secretion of anaphylatoxins C3a and C5a. This anaphylatoxin along with C5B-9 may trigger potentiate cytokine storm, leukocyte activation and their infiltration in alveolar cells of lungs. Thereby dysregulated complement system further deteriorates the pathologic condition elevating the severity. CP classical pathway, AP alternative pathway, LP Lectin pathway, N protein nucleocapsid protein, S protein spike protein, MASP2 : MBL Mannan-binding lectin serine protease 1, MBL Mannan-binding lectin, C3a/C5a complement activators C5/C3, MAC membrane attack complex, GM-CSF IL interleukins, TNF tumor necrosis factor, INF interferons

Article Snippet: LP involves binding of MBL (mannan-binding lectin, ficolins) with carbohydrate arrays belonging to mannan and N -acetylglucosamine residues located on either viral surface or pathogen infected cell-surface that in turn stimulates MBL-associated serine protease-2 (MASP-2), a MBL related protease acknowledged for direct initiation of complement system cascade [ ] (Fig. ).

Techniques: Infection, Activation Assay, Binding Assay, Membrane