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Fig. 1 | Beni-Suef University Journal of Basic and Applied Sciences

Fig. 1

From: Coinfection of fungi with SARS-CoV-2 is a detrimental health risk for COVID-19 patients

Fig. 1

An overview of how fungi take the chances of the hampered immune system caused by SARS-CoV-2. Innate immune response in SARS-CoV-2 infection: SARS-CoV-2 enter the host cell through the attachment of viral spike (S) protein to ACE-2 (angiotensin-converting enzyme-2) receptor on the cell membrane (1). Then ssRNA virus is reassembled to the dsRNA viral genome (2). TLR-3 (Toll-like receptor-3) mutation stops the NF-κβ (nuclear factor kappa-light-chain-enhancer of activated B cells) pathway and prevents the release of cytokines and chemokines (3). Macrophage releases IL-6, IL-10, IL-12, IL-18, IL1-β, and TNF-α (4). Antigen-presenting cells (APC) present MHC II (major histocompatibility complex II) peptide complex on T cells (5, 6). Adaptive immune response in SARS-CoV-2 infection: TH1/CD8 + and TH2/CD4 + release IFN-γ, TNF-α, IL-10, and IL-17 (7, 8). TH2 releases antibodies followed by activating B-cell (9, 10). Antibodies activate NK (natural killer) cells to release cytokines and chemokines (11, 12). Innate immune response in fungal infection after SARS-CoV-2 infection: Fungal complement protein stops the release of IL-6 and TGF-β (13). Fungal pathogens activate neutrophils (14). Pathogen attaches by dectin-1 in dendritic cells, and destructed immune system fails to release cytokines (15, 16). Pathogen escapes and subsequently presents on APC (antigen-presenting cells) with the help of the MHC II peptide complex to activate T cells (17, 18). Adaptive immune response in fungal infection after SARS-CoV-2 infection: Impaired adaptive immune response having cytokines from the “cytokine storm” results in the blockage of the proliferation of T cell into TH1/CD8 + and TH2/CD4 + (19, 20)

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