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. 2021 May 29;2:100102. doi: 10.1016/j.sintl.2021.100102

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© 2021 The Authors

Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

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Fig. 1 — Acute Immune Responses to Coronaviruses: To infect the cell, coronavirus gets entry inside the cell by binding to the ACE2 receptor. After entry, they sensitize the MMAVS & TLR3/7 receptors that upregulate the replication of pro-inflammatory genes (NF-κB), leading to increased cytokines and interferon production. Dendritic cells recognize the antigen and transfer to the lymphoid tissues to prime adaptive immunity. After recognizing the antigen on DCs or infected cells surface, CD8-T cells stimulate apoptosis. This mechanistic figure illustrates different steps where AS-CDs might produce theranostic activity. 1. Entry of coronavirus into the cell through binding ACE2 receptor. 2. Coronavirus initiate replication cycle inside the host cell. 3. Triggers the cytokine regulatory proteins (NF-κB, IRFs). 4. Induced protein incites the production of inflammatory cytokines. 5. Release of inflammatory cytokines. 6. Degradation of the cellular receptor. 7. Induction of cell apoptosis. The figure was created with BioRender.com.